Mechanoregulation of the Myofibroblast in Wound Contraction, Scarring, and Fibrosis: Opportunities for New Therapeutic Intervention
Open accessAbstract
SIGNIFICANCE: Myofibroblasts are responsible for wound closure that occurs in healed acute wounds. However, their actions can result in disfiguring scar contractures, compromised organ function, and a tumor promoting stroma. Understanding the mechanisms regulating their contractile machinery, gene expression, and lifespan is essential to develop new therapies to control their function. RECENT ADVANCES: Mechanical stress and transforming growth factor beta-1 (TGF-β1) regulate myofibroblast differentiation from mesenchymal progenitors. As these precursor cells differentiate, they assemble a contractile apparatus to generate the force used to contract wounds. The mechanisms by which mechanical stress promote expression of contractile genes through the TGF-β1 and serum response factor pathways and offer therapeutic targets to limit myofibroblast function are being elucidated. CRITICAL ISSUES: Emerging evidence suggests that the integration of mechanical cues with intracellular signaling pathways is critical to myofibroblast function via its effects on gene expression, cellular contraction, and paracrine signaling with neighboring cells. In addition, while apoptosis is clearly one pathway that can limit myofibroblast lifespan, recent data suggest that pathogenic myofibroblasts can become senescent and adopt a more beneficial phenotype, or may revert to a quiescent state, thereby limiting their function. FUTURE DIRECTIONS: Given the important role that myofibroblasts play in pathologies as disparate as cutaneous scarring, organ fibrosis, and tumor progression, knowledge gained in the areas of intracellular signaling networks, mechanical signal transduction, extracellular matrix biology, and cell fate will support efforts to develop new therapies with a wide impact.
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Myofibroblasts contribute to remodeling by releasing MMPs that degrade collagen laid down during granulation tissue formation.
“In addition to contraction of wound beds and generation of collagen, myofibroblasts contribute to remodeling by release of MMPs that degrade collagen laid down during granulation tissue formation [96, 97].”
From Immunology of Wound Healing (2018) · cites this paper as [97]
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- Authors
- Van De Water, L., Varney, S., & Tomasek, J. J.
- Affiliations
- Center for Cell Biology and Cancer Research, Albany Medical College, Albany, New York.
- Albany Medical College (US)
- University of Oklahoma Health Sciences Center (US)
- Venue
- Advances in Wound Care
- Publisher
- SAGE Publications
- Published
- 2013-05
- Volume
- 2
- Issue
- 4
- Pages
- 122-141
- ISSN
- 2162-1918 (ISSN-L)
- 2162-1934
- PMC
- PMC3656629
- OpenAlex
- W2168708680
- Cited by
- 251
- References
- 170
- Citations by year
- 2026: 12 · 2025: 19 · 2024: 20 · 2023: 24 · 2022: 20 · 2021: 35 · 2020: 17 · 2019: 24 · 2018: 20 · 2017: 20 · 2016: 17 · 2015: 13 · 2014: 9 · 2013: 1
- FWCI
- 2.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Advances in Wound Care (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Rensselaer Polytechnic Institute
- National Institutes of Health
- National Institute of General Medical Sciences
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- myofibroblasts, wound contraction, scar formation, fibrosis, mechanoregulation, mechanical stress, TGF-β1, serum response factor, myofibroblast differentiation, mesenchymal progenitor cells, contractile machinery, paracrine signaling, cellular senescence, apoptosis, extracellular matrix, tumor stroma, therapeutic target
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