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Myofibroblasts, contractile cells arising during repair, express α-smooth muscle actin and sustain pathological activation, overproducing ECM and promoting fibrotic progression. Beyond ECM deposition, myofibroblasts shape the tumor microenvironment (TME) by coordinating inflammation, angiogenesis, and tissue remodeling. Review evidence summarizes preclinical and clinical strategies to provoke myofibroblast death and restore TME remodeling across multiple fibrotic disease models and solid tumors.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/provoking-myofibroblast-death-strategies-to-resolve-fibrosis-and-remodel-tumor-microenvironment/406284/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/provoking-myofibroblast-death-strategies-to-resolve-fibrosis-and-remodel-tumor-microenvironment/406284.png","ImageObject",300,407,{"name":92,"@type":93},"Melati","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-05","2026-09-28",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What is the role of myofibroblasts in fibrosis and why is their apoptosis important?","Question",{"text":113,"@type":114},"Myofibroblasts are contractile cells that maintain persistent activation after injury, driving excessive ECM deposition and tissue stiffening. Provoking myofibroblast death is presented as a strategy to resolve fibrosis and prevent progressive dysfunction.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How do myofibroblasts influence the tumor microenvironment (TME)?",{"text":118,"@type":114},"Myofibroblasts contribute to the TME by interacting with immune cells, blood vessels, stromal cells, and ECM components surrounding cancer cells. Through these interactions, they modulate inflammation, angiogenesis, and tissue remodeling, affecting tumor growth and therapy responsiveness.",{"name":120,"@type":111,"acceptedAnswer":121},"Which disease models does the review discuss for targeting myofibroblasts?",{"text":122,"@type":114},"The review examines fibrotic and TME contexts across multiple disease models, including hypertrophic scar, idiopathic pulmonary fibrosis, oral submucous fibrosis, cardiac fibrosis, and the desmoplastic stroma in pancreatic and breast cancers.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},406284,1790822322,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146,"preview_page_count":4},962085570644,"https://ap-avatar.wpscdn.com/davatar_994ba38a5ba835b3df7d355c54d3ed8d","| W | J | C | O | World Journal of\u003Cbr>Clinical Oncology |\n| --- | --- | --- | --- | --- |\n\nSubmit a Manuscript: [https://www.f6publishing.com](https://www.f6publishing.com) World J Clin Oncol 2025 December 24; 16(12): 111086  \nDOI: 10.5306/wjco.v16.i12.111086 ISSN 2218-4333 (online)  \nMINIREVIEWS  \nProvoking myofibroblast death: Strategies to resolve fibrosis andremodel tumor microenvironment  \nThangavelu Shalini, Ganapasam Sudhandiran  \nSpecialty type: Oncology  \nProvenance and peer review:  \nInvited article; Externally peer reviewed.  \nPeer-review model: Single blind  \nPeer-review report’s classification Scientific Quality: Grade A, Grade B  \nNovelty: Grade B, Grade B  \nCreativity or Innovation: Grade B, Grade B  \nScientific Significance: Grade B, Grade B  \nP-Reviewer: Chen YZ, PhD, Postdoctoral Fellow, China  \nReceived: June 23, 2025  \nRevised: July 28, 2025  \nAccepted: November 13, 2025  \nPublished online: December 24, 2025  \nProcessing time: 183 Days and 18 Hours  \nThangavelu Shalini, Department of Biochemistry, University of Madras, Chennai 600025, Tamil Nādu, India  \nGanapasam Sudhandiran, Cell Biology Laboratory, Department of Biochemistry, University of Madras, Chennai 600025, Tamil Nādu, India  \nCorresponding author: Ganapasam Sudhandiran, PhD, Professor, Cell Biology Laboratory, Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600025, Tamil Nādu, [India.](India. sudhandiran@yahoo.com)[ sudhandiran@yahoo.com](India. sudhandiran@yahoo.com)  \nAbstract  \nFibrosis 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 of α-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 fibroticand 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.  \nKey Words: Myofibroblast apoptosis; Fibrosis resolution; Tumor microenvironment; Extracellular matrix remodeling; Fibroblast activation; Cancer-associated fibroblasts; Mechanotransduction in fibrosis  \n©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.  \n WJCO  [https://www.wjgnet.com](https://www.wjgnet.com) 1 December 24, 2025  Volume 16  Issue 12   \nShalini T et al. Myofibroblast in fibrosis and TME  \nCore Tip: Myofibroblasts are contractile cells that play a central role in both fibrosis and tumor progression due to their involvement in excessive extracellular matrix deposition and tissue stiffening. This article highlights emerging strategies to selectively inactivate or induce myofibroblast death, aiming to resolve fibrosis and remodel the tumor microenvironment. By exploring diverse disease models of fibrosis and cancer, this review underscores the therapeutic potential of targeting myofibroblasts to halt chronic tissue damage and improve cancer treatment outco","cbCain0TCD12CwZU","https://ap.wps.com/l/cbCain0TCD12CwZU","pdf",2444899,13,"English","# Abstract\n## Core Tip\n## Introduction","[{\"question\":\"What is the role of myofibroblasts in fibrosis and why is their apoptosis important?\",\"answer\":\"Myofibroblasts are contractile cells that maintain persistent activation after injury, driving excessive ECM deposition and tissue stiffening. Provoking myofibroblast death is presented as a strategy to resolve fibrosis and prevent progressive dysfunction.\"},{\"question\":\"How do myofibroblasts influence the tumor microenvironment (TME)?\",\"answer\":\"Myofibroblasts contribute to the TME by interacting with immune cells, blood vessels, stromal cells, and ECM components surrounding cancer cells. Through these interactions, they modulate inflammation, angiogenesis, and tissue remodeling, affecting tumor growth and therapy responsiveness.\"},{\"question\":\"Which disease models does the review discuss for targeting myofibroblasts?\",\"answer\":\"The review examines fibrotic and TME contexts across multiple disease models, including hypertrophic scar, idiopathic pulmonary fibrosis, oral submucous fibrosis, cardiac fibrosis, and the desmoplastic stroma in pancreatic and breast cancers.\"}]","Provoking myofibroblast death - Strategies to resolve fibrosis and remodel tumor microenvironment | PDF",1790564616,33]