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Effects of Oxidized Low Density Lipoprotein on Transformation of Valvular Myofibroblasts to Osteoblast-like Phenotype 认领 引用 被引量：2
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作者 陈娣 沈迎念 +2 位作者 胡伟林 陈正平 李永胜 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 2015年第3期362-367,共6页
In order to investigate the roles of Wnt signal pathway in transformation of cardiac valvular myofibroblasts to the osteoblast-like phenotype, the primary cultured porcine aortic valve myofibroblasts were incubated wi... In order to investigate the roles of Wnt signal pathway in transformation of cardiac valvular myofibroblasts to the osteoblast-like phenotype, the primary cultured porcine aortic valve myofibroblasts were incubated with oxidized low density lipoprotein（ox-LDL, 50 mg/L）, and divided into four groups according to the ox-LDL treatment time： control group, ox-LDL 24-h group, ox-LDL 48-h group, and ox-LDL 72-h group. Wnt signal pathway blocker Dickkopf-1（DDK-1, 100 μg/L） was added in ox-LDL 72-h group. The expression of α-smooth muscle actin（α-SMA）, bone morphogenetic protein 2（BMP2）, alkaline phosphatase（ALP）, and osteogenic transcription factor Cbfa-1 was detected by Western blotting, and that of β-catenin, a key mediator of Wnt signal pathway by immunocytochemical staining method. The Wnt/β-catenin was observed and the transformation of myofibroblasts to the osteoblast-like phenotype was examined. The expression of α-SMA, BMP2, ALP and Cbfa-1 proteins in the control group was weaker than in the ox-LDL-treated groups. In ox-LDL-treated groups, the protein expression of α-SMA, BMP2, ALP, and Cbfa-1 was significantly increased in a time-dependent manner as compared with the control group, and there was significant difference among the three ox-LDL-treated groups（P〈0.05 for all）; β-catenin protein was also up-regulated in the ox-LDL-treated groups in a time-dependent manner as compared with the control group（P〈0.05）, and its transfer from cytoplasm to nucleus and accumulation in the nucleus were increased in the same fashion（P〈0.05）. After addition of DKK-1, the expression of α-SMA, bone-related proteins and β-catenin protein was significantly reduced as compared with ox-LDL 72-h group（P〈0.05）. The Wnt/ β-catenin signaling pathway may play an important role in transformation of valvular myofibroblasts to the osteoblast-like phenotype. 展开更多
关键词 oxidized low density lipoprotein cardiac valve calcification myofibroblasts Wnt/β-catenin osteoblasts
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A red wine polyphenolic extract reduces the activation phenotype of cultured human liver myofibroblasts 认领 引用 被引量：1
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作者 Véronique Neaud Jean Rosenbaum 《World Journal of Gastroenterology》 SCIE CAS 2008年第14期2194-2199,共6页
AIM:To test the effect of a standardized red wine polyphenolic extract(RWPE)on the phenotype of human liver myofibroblasts in culture.METHODS:Human myofibroblasts grown from liver explants were used in this study.Cell... AIM:To test the effect of a standardized red wine polyphenolic extract(RWPE)on the phenotype of human liver myofibroblasts in culture.METHODS:Human myofibroblasts grown from liver explants were used in this study.Cell proliferation was measured with the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide(MTT)assay.Signaling events were analyzed by western blot with phosphospecific antibodies.Matrix-metalloproteinase activity was measured with gel zymography.RESULTS:We found that cell proliferation was dose-dependently decreased by up to 90%by RWPE while cell viability was not affected.Exposure to RWPE also greatly decreased the phosphorylation of ERK1/ERK2 and Akt in response to stimulation by the mitogenic factor platelet-derived growth factor BB(PDGF-BB).Finally,RWPE affected extracellular matrix remodeling by decreasing the secretion by myofibroblasts of matrix-metalloproteinase-2 and of tissue inhibitor of matrix-metalloproteinases-1.CONCLUSION:Altogether,RWPE decreases the activation state of liver myofibroblasts.The identification of the active compounds in RWPE could offer new therapeutic strategies against liver fibrosis. 展开更多
关键词 Liver fibrosis Myofibroblasts Hepatic stellate cells Wine Phosphorylation Proliferation
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Dynamic role of myofibroblasts in oral lesions 认领 引用 被引量：2
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作者 Neeta Bagul Anjali Ganjre +2 位作者 SN Goryawala Rahul Kathariya Shrikant Dusane 《World Journal of Clinical Oncology》 2015年第6期264-271,共8页
Fibroblasts are the most abundant cellular components of connective tissue. They possess phenotypical heterogenicity and may be present in the form of smooth muscle cells or myofibroblasts(MFs). MFs are spindle-shaped... Fibroblasts are the most abundant cellular components of connective tissue. They possess phenotypical heterogenicity and may be present in the form of smooth muscle cells or myofibroblasts(MFs). MFs are spindle-shaped cells with stress fibres and welldeveloped fibronexus,and they display α-smooth muscle actin immunohistochemically and smoothmuscle myofilaments ultrastructurally. MFs play a crucial role in physiological and pathological processes. Derived from various sources,they play pivotal roles not only by synthesizing and producing extracellular matrix components,such as other connective tissue cells,but also are involved in force production. In the tissue remodelling phase of wound closure,integrinmediated interactions between MFs and type I collagen result in scar tissue formation. The tumour stroma in oral cancer actively recruits various cell types into the tumour mass,where they act as different sources of MFs. This article reviews the importance of MFs and its role in pathological processes such as wound healing,odontogenic cysts and tumours,salivary gland tumours,oral preneoplasia,and oral squamous cell carcinoma. Research oriented on blocking the transdifferentiation of fibroblasts into MFs can facilitate the development of noninvasive therapeutic strategies for the treatment of fibrosis and/or cancer. 展开更多
关键词 Myofibroblasts Neoplasm Fibroblasts Precancerous lesions Carcinoma-associated fibroblasts Precancerous conditions
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An Improved Assay for Measuring Low Levels of Nitric Oxide in Cultured Pulmonary Myofibroblasts 认领 引用
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作者 Bethel V. Sharma Naomi S. Rowland +1 位作者 Margaret M. Clouse Nancy A. Rice 《Advances in Biological Chemistry》 CAS 2014年第3期214-221,共8页
Quantification of nitric oxide (NO) from cultured cells is a valuable tool for studying cell signaling. Detection of NO in biological fluids can be difficult however, due to its transient half-life and low physiologic... Quantification of nitric oxide (NO) from cultured cells is a valuable tool for studying cell signaling. Detection of NO in biological fluids can be difficult however, due to its transient half-life and low physiological concentrations. In this study, we have refined an existing amperometric method to determine relative levels of accumulated nitrogen oxides (NOX) in cell culture and have used this method to reproducibly quantify NO from cultured pulmonary myofibroblasts. Basal levels of NO produced by pulmonary myofibroblasts ranged from 0.6 nM to 20 nM and varied due to the growth conditions of the cells, i.e. higher NO concentrations were observed in differentiated cells. The constitutive eNOS isoform is primarily responsible for the observed NO accumulation in these cells since transcript levels of eNOS are 10-fold higher than the inducible iNOS form while nNOS was undetectable. Treatment of myofibroblasts with the inhibitors L-NNA and L-NAME resulted in a concentration dependent decrease in measured NOx. Overall, the improved assay presented here should be applicable to measuring NOX levels from many different cell types and under a wide variety of conditions. 展开更多
关键词 Myofibroblast Pulmonary Nitric Oxide eNOS
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RDYH58 functional exosomes targeting myofibroblasts loaded with siFKBP10 for inhibition of collagen biosynthesis and secretion of IPF 认领 引用 被引量：2
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作者 Ranran Yuan Zhen Mu +12 位作者 Houqian Zhang Yu Tian Quanlin Xin Qingchao Tu Yan Zhang Yanqiu Li Zhiwen Zhang Yongchao Chu Aiping Wang Jingwei Tian Hongbo Wang Chong Qiu Yanan Shi 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2025年第12期6681-6697,共17页
Idiopathic pulmonary fibrosis(IPF)is a complex interstitial lung disease in which myofibroblasts are the primary effector cells.FK506-binding protein(FKBP10),a procollagen chaperone,is upregulated in IPF and primarily... Idiopathic pulmonary fibrosis(IPF)is a complex interstitial lung disease in which myofibroblasts are the primary effector cells.FK506-binding protein(FKBP10),a procollagen chaperone,is upregulated in IPF and primarily localizes to myofibroblasts.Exosomes have garnered significant attention as novel drug delivery vehicles,particularly when engineered.However,myofibroblasts remain underexplored in terms of engineered exosome-based therapies and associated drug targets.In this study,RDYH58,a peptide that targets myofibroblasts,was conjugated to the exosomal membrane protein Lamp2b to produce RDYH58-linked exosomes(RDYH58-exo).In vitro and in vivo experiments demonstrated that compared to unmodified exosomes(unm-exo),RDYH58-exo preferentially localized to myofibroblasts.A small interfering RNA targeting FKBP10(siFKBP10)was loaded into exosomes using ultrasonic microfluidics method,and the antifibrotic effects of RDYH58-exo carrying siFKBP10(RDYH58-siFKBP10)were assessed both in vitro and in vivo.The results demonstrated that RDYH58-siFKBP10 effectively silenced FKBP10 gene expression,significantly inhibiting fibroblast activation and extracellular matrix deposition,with superior antifibrotic efficacy compared to unmodified exosome vectors(unm-siFKBP10).RNA-seq analysis confirmed the pivotal regulatory role of FKBP10,providing critical evidence for the development of targeted therapeutic strategies.The RDYH58-siFKBP10 delivery system developed in this study demonstrates remarkable clinical translation potential. 展开更多
关键词 Idiopathic pulmonary fibrosis Myofibroblasts FK506-Binding protein RDYH58 Exosomes Drug delivery Small interfering RNA Ultrasonic microfluidics method
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Hydrogen sulfide suppresses transforming growth factor-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts 认领 引用 被引量：12
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作者 ZHANG YouEn WANG JiaNing +4 位作者 LI Hua YUAN LiangJun WANG Lei WU Bing GE JunBo 《Science China(Life Sciences)》 SCIE CAS CSCD 2015年第11期1126-1134,共9页
In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investi... In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure. 展开更多
关键词 human cardiac fibroblasts hydrogen sulfide transforming growth factor β1 myofibroblasts
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Modulating hepatic stellate cell senescence:A promising therapeutic strategy for liver fibrosis 认领 引用
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作者 Muthusethupathi Sharmila Karthik Shree Harini Devaraj Ezhilarasan 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS CSCD 2026年第4期382-393,共12页
Fibrosis is characterized by the abnormal deposition of extracellular matrix(ECM)components in liver tissue following chronic liver injury,ultimately leading to hepatic cirrhosis.Following liver damage,hep-atic stella... Fibrosis is characterized by the abnormal deposition of extracellular matrix(ECM)components in liver tissue following chronic liver injury,ultimately leading to hepatic cirrhosis.Following liver damage,hep-atic stellate cells(HSCs)undergo transition from a quiescent to an activated phenotype which differen-tiate into proliferative,fibrogenic,and contractile myofibroblasts.The activated HSCs act as the primary source of collagen in the injured liver,promoting scar formation and fibrogenesis while reducing ECM degradation.Therefore,potential therapeutic strategies for liver fibrosis include inhibiting HSC activation,proliferation,and function,as well as promoting their clearance through autophagy,pro-apoptotic agents,and senescence inducers.In recent years,the induction of HSC senescence has emerged as a promising therapeutic approach to halt fibrosis progression.This review provided a comprehensive analysis of the fundamental role of the senescence-associated secretory phenotype and its regulatory pathways,includ-ing cyclic GMP-AMP synthase-stimulator of interferon genes,Notch signaling,nuclear factor kappa B,and mechanistic target of rapamycin complexes.This review also discussed each of these pathways in terms of their influence on the senescence behaviour of HSCs and their interactions within the fibrotic hepatic microenvironment.Recent advancements in identifying senescence markers,such as p21,β-galactosidase,interleukin-6,and urokinase plasminogen activator receptor,offer promising opportunities for targeted therapeutic interventions.Consequently,the strategic targeting of HSC senescence emerges as a com-pelling therapeutic approach for liver fibrosis,with the potential not only to halt disease progression but also to promote essential tissue remodeling processes. 展开更多
关键词 Myofibroblasts Liver fibrosis Cirrhosis Chronic liver injury Health Disease
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Pharmacological regulation of tissue fibrosis by targeting the mechanical contraction of myofibroblasts 认领 引用
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作者 Zheng-Quan He Xue-Wei Yuan +7 位作者 Zong-Bao Lu Yu-Huan Li Yu-Fei Li Xin Liu Liu Wang Ying Zhang Qi Zhou Wei Li 《Fundamental Research》 CAS 2022年第1期37-47,共11页
Fibrosis can occur in almost all tissues and organs and affects normal physiological function,which may have serious consequences,such as organ failure.However,there are currently no effective,broad-spectmm drugs suit... Fibrosis can occur in almost all tissues and organs and affects normal physiological function,which may have serious consequences,such as organ failure.However,there are currently no effective,broad-spectmm drugs suitable for clinical application.Revealing the process of fibrosis is an important prerequisite for the development of new therapeutic targets and drugs.Studies have shown that the limiting of myofibroblast activation or the promoting of their elimination can ameliorate fibrosis.However,it has not been reported whether a direct decrease in cell contraction can inhibit fibrosis in vivo.Here,we have shown that(-)-blebbistatin(Ble),a non-muscle myosin II inhibitor,displayed significant inhibition of liver fibrosis in different chronic injury mouse models in vivo.We found that Ble reduced the stiffness of fibrotic tissues from the early stage,which reduced the extent of myofibroblast activation induced by a stiffer extracellular matrix(ECM).Moreover,Ble also reduced the activation of myofibroblasts induced by TGF-β1,which is the most potent pro-fibrotic cytokine.Mechanistically,Ble reduced mechanical contraction,which inhibited the assembly of stress fibers,decreased the F/G-actin ratio,and led to the exnucleation of YAPJ and MRTF-A.Finally,we verified its broad-spectrum antifibrotic effect in multiple models of organ fibrosis.Our results highlighted the important role of mechanical contraction in myofibroblast activation and maintenance,rather than just a characteristic of activation,suggesting that it may be a potential target to explore broad-spectrum drugs for the treatment of fibrotic diseases. 展开更多
关键词 Fibrosis Myofibroblasts Contraction Inhibitor Biomechanics Regeneration
Role of oxygen free radicals in the proliferation of myofibroblasts induced by AngII 认领 引用
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作者 Liying Wang Hong Li Shijie Yang 《Acta Pharmaceutica Sinica B》 SCIE CAS 2013年第1期32-37,共6页
Previous studies have demonstrated the important role of angiotension II(AngII)in promoting proliferation of myofibroblasts(myoFbs)and myocardial fibrosis.However,the underlying mechanisms and the role of oxygen free ... Previous studies have demonstrated the important role of angiotension II(AngII)in promoting proliferation of myofibroblasts(myoFbs)and myocardial fibrosis.However,the underlying mechanisms and the role of oxygen free radicals in the proliferation of myofibroblasts induced by AngII are unclear.The present study was designed to shed light on this issue through exploration of AngII signaling pathways via in vitro experiments.Primary cultures of neonatal rat myoFbs were divided into five groups which were treated with AngII(10-8 to 10-6 M),AngII with the antioxidant N-acetyl-L-cysteine(NAC),or normal culture medium.We observed the proliferation of myoFbs as induced by AngII at different concentrations with MTT.Reactive oxygen species(ROS)levels in myoFbs were detected by monitoring the fluorescence of 2',7'-dichlorofluorescein.The contents and levels of oxygen free radicals(OH·)in the three groups were detected by spectrophotometer,immunocytochemical staining,and confocal fluorescence.Western blot and image analysis were used to measure membrane translocation and expression of phospho-protein kinase Ca.MyoFbs incubated with AngII(10-8 to 10-6 M)for 24 h increased their rate of proliferation,the content of OH·,and expression of ROS(P<0.01 vs.control group),whereas these parameters decreased in the presence of NAC.Immunocytochemistry,confocal fluorescence staining and image analysis showed that AngII could promote the translocation and expression of p-PKCα in membrane,and the antioxidant NAC blocked this increase(P<0.01).Western blot results also showed that NAC could inhibit the expression of p-PKCα. 展开更多
关键词 N-acetyl-L-cysteine AngII Oxygen free radical Myofibroblasts Protein kinase Ca
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Clinical features and prognosis of orbital inflammatory myofibroblastic tumor 认领 引用
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作者 Jing Li Liang-Yuan Xu +9 位作者 Nan Wang Rui Liu Shan-Feng Zhao Ting-Ting Ren Qi-Han Guo Bin Zhang Hong Zhang Hai-Han Yan Yu-Fei Zhang Jian-Min Ma 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第1期105-114,共10页
AIM:To investigate the clinical features and prognosis of patients with orbital inflammatory myofibroblastic tumor(IMT).METHODS:This retrospective study collected clinical data from 22 patients diagnosed with orbital ... AIM:To investigate the clinical features and prognosis of patients with orbital inflammatory myofibroblastic tumor(IMT).METHODS:This retrospective study collected clinical data from 22 patients diagnosed with orbital IMT based on histopathological examination.The patients were followed up to assess their prognosis.Clinical data from patients,including age,gender,course of disease,past medical history,primary symptoms,ophthalmologic examination findings,general condition,as well as imaging,laboratory,histopathological,and immunohistochemical results from digital records were collected.Orbital magnetic resonance imaging(MRI)and(or)computed tomography(CT)scans were performed to assess bone destruction of the mass,invasion of surrounding tissues,and any inflammatory changes in periorbital areas.RESULTS:The mean age of patients with orbital IMT was 28.24±3.30y,with a male-to-female ratio of 1.2:1.Main clinical manifestations were proptosis,blurred vision,palpable mass,and pain.Bone destruction and surrounding tissue invasion occurred in 72.73%and 54.55%of cases,respectively.Inflammatory changes in the periorbital site were observed in 77.27%of the patients.Hematoxylin and eosin staining showed proliferation of fibroblasts and myofibroblasts,accompanied by infiltration of lymphocytes and plasma cells.Immunohistochemical staining revealed that smooth muscle actin(SMA)and vimentin were positive in 100%of cases,while anaplastic lymphoma kinase(ALK)showed positivity in 47.37%.The recurrence rate of orbital IMT was 27.27%,and sarcomatous degeneration could occur.There were no significant correlations between recurrence and factors such as age,gender,laterality,duration of the disease,periorbital tissue invasion,bone destruction,periorbital inflammation,tumor size,fever,leukocytosis,or treatment(P>0.05).However,lymphadenopathy and a Ki-67 index of 10%or higher may be risk factors for recurrence(P=0.046;P=0.023).CONCLUSION:Orbital IMT is a locally invasive disease that may recur or lead to sarcomatoid degeneration,primarily affecting young and middle-aged patients.The presence of lymphadenopathy and a Ki-67 index of 10%or higher may signify a poor prognosis. 展开更多
关键词 inflammatory myofibroblastic tumor orbital disease clinical features prognosis
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Ultrasonographic Findings of Low-Grade Myofibroblastic Sarcoma:A Case Report 认领 引用
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作者 Guoxin Huang Dejuan Shen 《Journal of Clinical and Nursing Research》 2026年第4期280-284,共5页
Objective:To analyze the ultrasonographic features of low-grade myofibroblastic sarcoma(LGMS)and explore its preoperative diagnostic value and key points of differential diagnosis.Methods:A case of LGMS confirmed by s... Objective:To analyze the ultrasonographic features of low-grade myofibroblastic sarcoma(LGMS)and explore its preoperative diagnostic value and key points of differential diagnosis.Methods:A case of LGMS confirmed by surgical pathology was retrospectively analyzed.The ultrasonographic manifestations were combined with magnetic resonance imaging(MRI)and pathological results for comprehensive analysis,and relevant literature was reviewed.Results:The patient was a 41-year-old female with a hypoechoic mass(45 mm×30 mm×21 mm)in the muscle layer of the left lower leg.The mass had an irregular shape with lobulated margins,and some boundaries were unclear.A large hyperechoic area(8.0 mm×1.6 mm)was seen inside.Color Doppler flow imaging(CDFI)showed rich blood supply around and within the mass,and a cord-like extension was visible at the lower edge.MRI showed an isointense signal on T1-weighted images and a long T2 signal,with high signal intensity on diffusion-weighted imaging(DWI)and significant enhancement on contrast-enhanced scans.Postoperative pathology confirmed LGMS.Conclusion:The ultrasonographic manifestations of LGMS have certain characteristics,but a definite diagnosis still depends on pathological examination.Ultrasonography can provide important imaging evidence for preoperative assessment. 展开更多
关键词 Ultrasonography Low-grade myofibroblastic sarcoma Soft tissue tumor Color Doppler flow imaging Magnetic resonance imaging Differential diagnosis
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Subretinal fibrosis secondary to neovascular age-related macular degeneration:mechanisms and potential therapeutic targets 认领 引用 被引量：3
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作者 Jingxiang Zhang Xia Sheng +3 位作者 Quanju Ding Yujun Wang Jiwei Zhao Jingfa Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第2期378-393,共16页
Subretinal fibrosis is the end-stage sequelae of neovascular age-related macular degeneration.It causes local damage to photoreceptors,retinal pigment epithelium,and choroidal vessels,which leads to permanent central ... Subretinal fibrosis is the end-stage sequelae of neovascular age-related macular degeneration.It causes local damage to photoreceptors,retinal pigment epithelium,and choroidal vessels,which leads to permanent central vision loss of patients with neovascular age-related macular degeneration.The pathogenesis of subretinal fibrosis is complex,and the underlying mechanisms are largely unknown.Therefore,there are no effective treatment options.A thorough understanding of the pathogenesis of subretinal fibrosis and its related mechanisms is important to elucidate its complications and explore potential treatments.The current article reviews several aspects of subretinal fibrosis,including the current understanding on the relationship between neovascular age-related macular degeneration and subretinal fibrosis;multimodal imaging techniques for subretinal fibrosis;animal models for studying subretinal fibrosis;cellular and non-cellular constituents of subretinal fibrosis;pathophysiological mechanisms involved in subretinal fibrosis,such as aging,infiltration of macrophages,different sources of mesenchymal transition to myofibroblast,and activation of complement system and immune cells;and several key molecules and signaling pathways participating in the pathogenesis of subretinal fibrosis,such as vascular endothelial growth factor,connective tissue growth factor,fibroblast growth factor 2,platelet-derived growth factor and platelet-derived growth factor receptor-β,transforming growth factor-βsignaling pathway,Wnt signaling pathway,and the axis of heat shock protein 70-Toll-like receptors 2/4-interleukin-10.This review will improve the understanding of the pathogenesis of subretinal fibrosis,allow the discovery of molecular targets,and explore potential treatments for the management of subretinal fibrosis. 展开更多
关键词 choroidal neovascularization epithelial-mesenchymal transition mesenchymal transition myofibroblast neovascular age-related macular degeneration submacular fibrosis subretinal fibrosis therapeutic targets transforming growth factor-β vascular endothelial growth factor
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Provoking myofibroblast death:Strategies to resolve fibrosis and remodel tumor microenvironment 认领 引用 被引量：1
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作者 Thangavelu Shalini Ganapasam Sudhandiran 《World Journal of Clinical Oncology》 2025年第12期67-78,共12页
Fibrosis is marked by the excessive accumulation of extracellular matrix(ECM)components,leading to tissue scarring and progressive loss of organ function.Myofibroblasts,which emerge during tissue repair,are specialize... Fibrosis is marked by the excessive accumulation of extracellular matrix(ECM)components,leading to tissue scarring and progressive loss of organ function.Myofibroblasts,which emerge during tissue repair,are specialized contractile cells exhibiting features of both fibroblasts and smooth muscle cells.Their expression ofα-smooth muscle actin facilitates contractile activity,while their persistent activation and overproduction of ECM components contribute significantly to pathological wound contraction and fibrotic progression.Beyond ECM production,myofibroblasts play a significant role in the tumor microenvironment(TME)of various solid tumors.The TME is a complex network of immune cells,blood vessels,ECM components,and stromal cells like fibroblasts and myofibroblasts that surrounds and interacts with cancer cells,thereby influencing tumor growth,progression,and therapy responsiveness.Through these interactions,myofibroblasts modulate inflammation,angiogenesis,and tissue remodeling.Maintaining myofibroblast homeostasis is therefore crucial,as its disruption can drive the onset of chronic fibrotic conditions and malignancies.This review explores preclinical and clinical developments in targeting myofibroblasts in fibrotic and TME across various disease models,including hypertrophic scar,idiopathic pulmonary fibrosis,oral submucous fibrosis,cardiac fibrosis,and the desmoplastic stroma of pancreatic and breast cancers. 展开更多
关键词 Myofibroblast apoptosis Fibrosis resolution Tumor microenvironment Extracellular matrix remodeling Fibroblast activation Cancer-associated fibroblasts Mechanotransduction in fibrosis
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Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells 认领 引用
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作者 Md Ariful Islam Jannatul Mawya +2 位作者 Umme Salma Noor Hayaty Abu Kasim Nazmul Haque 《World Journal of Stem Cells》 SCIE 2025年第11期9-26,共18页
Hepatic fibrosis is a pathological process characterized by an imbalance between the deposition and degradation of extracellular matrix components.This process is initiated by chronic liver injuries resulting from vir... Hepatic fibrosis is a pathological process characterized by an imbalance between the deposition and degradation of extracellular matrix components.This process is initiated by chronic liver injuries resulting from viral infections,alcoholic liver disease,non-alcoholic fatty liver disease,and autoimmune-mediated hepatic damage.If left untreated,hepatic fibrosis can progress to life-threatening conditions such as cirrhosis and hepatocellular carcinoma.Central to the development of fibrosis is the transdifferentiation of quiescent hepatic stellate cells(HSCs)into proliferative and fibrogenic myofibroblast-like activated HSCs(aHSCs),which play a crucial role in extracellular matrix accumulation and fibrotic tissue formation.Beyond resmetirom,a recently Food and Drug Administrationapproved medication for liver fibrosis and nonalcoholic steatohepatitis,there are currently no other established pharmacological treatments available to slow down the progression of these conditions.Moreover,activation of HSCs and formation of hepatic fibrosis have been considered irreversible.Recent studies reported transforming growth factor beta as one of the key regulators of HSCs activation and pathogenesis of hepatic fibrosis.It has been also reported that the features of aHSCs can be reversed to those of quiescent HSCs by modulating transforming growth factor beta mediated pathways.The potential of extracellular vesicles(EVs)as cell free therapeutics to treat hepatic fibrosis has been suggested earlier.However,detailed knowledge of the mechanisms involved in the alleviation of hepatic fibrosis using EVs from mesenchymal stem cells is still lacking.Hence,this review aims to describe the pathogenesis of hepatic fibrosis from the cellular and molecular point of views and shed light on the potential of EVs from mesenchymal stem cells in reversing the properties of aHSCs to their quiescent state. 展开更多
关键词 Exosomes MicroRNAs Myofibroblast Nuclear factor kappa B Transforming growth factor-beta
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High-grade myofibroblastic sarcoma in the first metacarpal:An unusual case in hand surgery 认领 引用
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作者 Osnaya-Moreno Humberto Jiménez-Murat Yusef +1 位作者 Ceballos-Villalva Jesús Carlos Fukumoto-Inukai Kenzo Alejandro 《Chinese Journal of Plastic and Reconstructive Surgery》 2025年第1期30-34,共5页
Myofibroblastic sarcoma(MS)is a rare malignant soft tissue tumor characterized by myofibroblasts.It most commonly arises in the head and neck region,especially the tongue,with rare occurrences in the limbs.MS exhibits... Myofibroblastic sarcoma(MS)is a rare malignant soft tissue tumor characterized by myofibroblasts.It most commonly arises in the head and neck region,especially the tongue,with rare occurrences in the limbs.MS exhibits varying histopathology,ranging from low-to high-grade,with diverse subtypes showing different clinical behaviors and prognoses.This article reports the first case of high-grade MS in the hand,adding to the limited documentation of this rare condition.Here,we present the case of a 30-year-old healthy female with a year-long history of progressive shortening,mobility loss,and weakness in the first finger of the left hand.Left-hand imaging revealed a lytic,cottony tumor involving the entire first metacarpal.Following surgical resection,which included metatarsal grafting and joint reconstruction,a diagnosis of high-grade MS was confirmed based on histological manifestations and immunohistochemical staining,which was further classified as grade 2 according to the French Federation of Cancer Centers Sarcoma Group system.Postoperative radiotherapy was administered and the patient experienced a successful recovery without graft osteonecrosis.The patient regained 90%mobility and strength,without shortening,after surgical resection and radiotherapy.Six months post-surgery,the patient reported full hand functionality.MS is a rare tumor that infrequently affects bones and is often misdiagnosed owing to its controversial characteristics.The initial treatment should focus on complete resection with negative margins,followed by reconstructive surgery to preserve function.Further case studies are needed to establish standardized surgical treatment protocols. 展开更多
关键词 Myofibroblastic sarcoma High-grade tumor Reconstructive surgery Metacarpal tumor
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Cellular and molecular mechanisms of intestinal fibrosis 认领 引用 被引量：38
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作者 Silvia Speca Ilaria Giusti +1 位作者 Florian Rieder Giovanni Latella 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第28期3635-3661,共27页
Fibrosis is a chronic and progressive process characterized by an excessive accumulation of extracellular matrix (ECM) leading to stiffening and/or scarring of the involved tissue. Intestinal fibrosis may develop in s... Fibrosis is a chronic and progressive process characterized by an excessive accumulation of extracellular matrix (ECM) leading to stiffening and/or scarring of the involved tissue. Intestinal fibrosis may develop in several different enteropathies, including inflammatory bowel disease. It develops through complex cell, extracellular matrix, cytokine and growth factor interactions. Distinct cell types are involved in intestinal fibrosis, such as resident mesenchymal cells (fibroblasts, myofibroblasts and smooth muscle cells) but also ECM-producing cells derived from epithelial and endothelial cells (through a process termed epithelialand endothelial-mesenchymal transition), stellate cells, pericytes, local or bone marrow-derived stem cells. The most important soluble factors that regulate the activation of these cells include cytokines, chemokines, growth factors, components of the renin-angiotensin system, angiogenic factors, peroxisome proliferator-activated receptors, mammalian target of rapamycin, and products of oxidative stress. It soon becomes clear that although inflammation is responsible for triggering the onset of the fibrotic proc-ess, it only plays a minor role in the progression of this condition, as fibrosis may advance in a self-perpetuating fashion. Definition of the cellular and molecular mechanisms involved in intestinal fibrosis may provide the key to developing new therapeutic approaches. 展开更多
关键词 Inflammatory bowel disease Intestinal fibrosis Extracellular matrix Molecular mediators Myofibroblasts Inflammatory cells Epithelial cells Mesenchymal cells Endothelial cells
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Transforming growth factor-β1 induces intestinal myofibroblast differentiation and modulates their migration 认领 引用 被引量：21
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作者 Julia Brenmoehl Sandra Nicole Miller +4 位作者 Claudia Hofmann Daniela Vogl Werner Falk Jrgen Schlmerich Gerhard Rogler 《World Journal of Gastroenterology》 SCIE CAS 2009年第12期1431-1442,共12页
AIM： To investigate the effects of transforming growth factor β1 （TGF-β1） on the differentiation of colonic lamina propria fibroblasts （CLPF） into myofibroblasts in vitro.METHODS： Primary CLPF cultures were in... AIM： To investigate the effects of transforming growth factor β1 （TGF-β1） on the differentiation of colonic lamina propria fibroblasts （CLPF） into myofibroblasts in vitro.METHODS： Primary CLPF cultures were incubated with TGF-β1 and analyzed for production of m-smooth muscle actin （α-SMA）, fibronectin （FN） and FN isoforms. Migration assays were performed in a modified 48-well Boyden chamber. Levels of total and phosphorylated focal adhesion kinase （FAK） in CLPF were analyzed after induction of migration.did not change α-SMA levels, while TGF-β1 treatment for 6 d significantly increased α-SIVlA production. Short term incubation （6 h） with TGF-β1 enhanced CLPF migration, while long term treatment （6 d） of CLPF with TGF-β1 reduced migration to 15%-37% compared to untreated cells. FN and FN isoform mRNA expression were increased after short term incubation with TGF-β1 （2 d） in contrast to long term incubation with TGF-β1 for 6 d. After induction of migration, TGF-β1-preincubated CLPF showed higher amounts of FN and its isoforms and lower levels of total and phosphorylated FAK than untreated cells.CONCLUSION： Long term incubation of CLPF with TGF-β1 induced differentiation into myofibroblasts with enhanced α-SMA, reduced migratory potential and FAK phosphorylation, and increased FN production. In contrast, short term contact （6 h） of fibroblasts with TGF-β1 induced a dose-dependent increase of cell migration and FAK phosphorylation without induction of α-SMA production. 展开更多
关键词 Transforming growth factor β1 Colonicfibroblasts Myofibroblasts Migration Fibronectin
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Thiazolidinedione treatment inhibits bile duct proliferation and fibrosis in a rat model of chronic cholestasis 认领 引用 被引量：11
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作者 Fabio Marra Raffaella DeFranco +10 位作者 Gaia Robino Erica Novo Eva Efsen Sabrina Pastacaldi Elena Zamara Alessandro Vercelli Benedetta Lottini Carlo Spirli Mario Strazzabosco Massimo Pinzani Maurizio Parola 《World Journal of Gastroenterology》 SCIE CAS 2005年第32期4931-4938,共8页
AIM： To investigate the effects of troglitazone （TGZ）, an anti-diabetic drug which activates peroxisome proliferatoractivated receptor-y （PPAR-y）, for liver tissue repair, and the development of ductular reaction... AIM： To investigate the effects of troglitazone （TGZ）, an anti-diabetic drug which activates peroxisome proliferatoractivated receptor-y （PPAR-y）, for liver tissue repair, and the development of ductular reaction, following common bile duct ligation （BDL） in rats. METHODS： Rats were supplemented with TGZ （0.2% w/w in the pelleted food） for i wk before BDL or sham operation. Animals were killed at 1, 2, or 4 wk after surgery. RESULTS： The development of liver fibrosis was reduced in rats receiving TGZ, as indicated by significant decreases of procollagen type I gene expression and liver hydroxyproline levels. Accumulation of a-smooth-muscle actin （SMA）-expressing cells surrounding newly formed bile ducts following BDL, as well as total hepatic levels of SMA were partially inhibited by TGZ treatment, indicating the presence of a reduced number and/or activation of hepatic stellate cells （HSC） and myofibroblasts. Development of the ductular reaction was inhibited by TGZ, as indicated by histochemical evaluation and hepatic activity of γ-glutamyltransferase （GGT）. CONCLUSION： Treatment with thiazolidinedione reduces ductular proliferation and fibrosis in a model of chronic cholestasis, and suggests that limiting cholangiocyte proliferation may contribute to the lower development of scarring in this system. 展开更多
关键词 Cholangiocytes Ductular reaction PPAR-γ Hepatic stellate cells Myofibroblasts Troglitazone
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Microstructural and ultrastructural changes in the healing process of bile duct trauma 认领 引用 被引量：18
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作者 Jun Xu Zhi-Min Geng Qing-Yong Ma the Department of Hepatobiliary Surgery, First Hospital of Xi’an Jiaotong University, Xi’an 710061, China 《Hepatobiliary & Pancreatic Diseases International》 CAS 2003年第2期611-615,共5页
OBJECTIVE: To explore the mechanism of benign biliary stricture caused by bile duct trauma. METHODS: A model of trauma of the common bile duct was established in 28 dogs and then repaired. The anastomotic tissues were... OBJECTIVE: To explore the mechanism of benign biliary stricture caused by bile duct trauma. METHODS: A model of trauma of the common bile duct was established in 28 dogs and then repaired. The anastomotic tissues were taken on 3 days, 1 week, 3 weeks, 3 months, and 6 months respectively after operation and examined by using light microscopy and electromicroscopy. Macrophage. transforming growth factor beta I (TGF-β1) and α-smooth muscle actin (α-SMA) were studied immunohistochemically. RESULTS: The mucosal epithelium of the common bile duct restored poorly, chronic inflammation lasted for a long time, fibroblasts proliferated actively, extracellular matrix overdeposited, and myofibroblasts functioned actively during the whole healing process. Immunohistochemical test showed a high expression of macrophage, TGF-β1 and α-SMA during the healing process lasting a long duration. Macrophages were found in the lamina propria under mucosa, TGF-β1 in the granular tissue, fibroblasts and endothelial cells of blood vessels, while α-SMA in the myofibroblasts and smooth muscle tissue. CONCLUSIONS: The healing of the bile duct is in the mode of overhealing. Myofibroblast is the main cause for contracture of scar and stricture of the bile duct. The high expression of macrophage, TGF-β1 and α-SMA is closely related to active proliferation of fibroblasts, extracellular matrix overdeposition and scar contracture of the bile duct. 展开更多
关键词 bile duct trauma stenosis wound healing myofibroblasts TGF-β1 α-SMA
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Protective Effect of Angiotensin(1-7) on Silicotic Fibrosis in Rats 认领 引用 被引量：5
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作者 ZHANG Bo Nan XU Hong +3 位作者 GAO Xue Min ZHANG Gui Zhen ZHANG Xin YANG Fang 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2019年第6期419-426,共8页
Objective Silicosis, caused by inhalation of silica dust, is the most serious occupational disease in China and the aim of present study was to explore the protective effect of Ang(1-7) on silicotic fibrosis and myofi... Objective Silicosis, caused by inhalation of silica dust, is the most serious occupational disease in China and the aim of present study was to explore the protective effect of Ang(1-7) on silicotic fibrosis and myofibroblast differentiation induced by Ang II. Methods HOPE-MED 8050 exposure control apparatus was used to establish the rat silicosis model. Pathological changes and collagen deposition of the lung tissue were examined by H.E. and VG staining, respectively. The localizations of ACE2 and α-smooth muscle actin(α-SMA) in the lung were detected by immunohistochemistry. Expression levels of collagen type I, α-SMA, ACE2, and Mas in the lung tissue and fibroblasts were examined by western blot. Levels of ACE2, Ang(1-7), and Ang II in serum were determined by ELISA. Co-localization of ACE2 and α-SMA in fibroblasts was detected by immunofluorescence. Results Ang(1-7) induced pathological changes and enhanced collagen deposition in vivo. Ang(1-7) decreased the expressions of collagen type I and α-SMA and increased the expressions of ACE2 and Mas in the silicotic rat lung tissue and fibroblasts stimulated by Ang II. Ang(1-7) increased the levels of ACE2 and Ang(1-7) and decreased the level of Ang II in silicotic rat serum. A779 enhanced the protective effect of Ang(1-7) in fibroblasts stimulated by Ang II. Conclusion Ang(1-7) exerted protective effect on silicotic fibrosis and myofibroblast differentiation induced by Ang II by regulating ACE2-Ang(1-7)-Mas axis. 展开更多
关键词 Silicosis Ang II Myofibroblasts Ang(1-7) A779
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