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The role of myofibroblasts in wound healing
Abstract
The importance of proper skin wound healing becomes evident when our body's repair mechanisms fail, leading to either non-healing (chronic) wounds or excessive repair (fibrosis). Chronic wounds are a tremendous burden for patients and global healthcare systems and are on the rise due to their increasing incidence with age and diabetes. Curiously, these same risk factors also sign responsible for the development of hypertrophic scarring and organ fibrosis. Activated repair cells - myofibroblasts - are the main producers and organizers of extracellular matrix which is needed to restore tissue integrity after injury. Too many myofibroblasts working for too long cause tissue contractures that ultimately obstruct organ function. Insufficient myofibroblast activation and activities, in turn, prevents normal wound healing. This short review puts a spotlight on the myofibroblast for those who seek therapeutic targets in the context of dysregulated tissue repair. "Keep your myofibroblasts in balance" is the message.
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“Recent evidence indicates that myofibroblast-induced fibrosis can be over-activated, not only in the setting of signaling through TGF-β, but also in the setting of Th2-derived cytokines IL-4 and IL-13; Th1 cytokines, such as IFN-γ, attenuate excessive scar formation [100, 101].”
From Immunology of Wound Healing (2018) · cites this paper as [101]
In the citing paper
“Recent evidence indicates that myofibroblast-induced fibrosis can be over-activated, not only in the setting of signaling through TGF-β, but also in the setting of Th2-derived cytokines IL-4 and IL-13; Th1 cytokines, such as IFN-γ, attenuate excessive scar formation [100, 101].”
From Immunology of Wound Healing (2018) · cites this paper as [101]
In the citing paper
“Recent evidence indicates that myofibroblast-induced fibrosis can be over-activated, not only in the setting of signaling through TGF-β, but also in the setting of Th2-derived cytokines IL-4 and IL-13; Th1 cytokines, such as IFN-γ, attenuate excessive scar formation [100, 101].”
From Immunology of Wound Healing (2018) · cites this paper as [101]
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Metadata
- Authors
- Hinz, B.
- Affiliations
- University of Toronto (CA)
- Corresponding author
- Hinz, B.
- ORCID
- Hinz, B.
- Venue
- Current Research in Translational Medicine
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 64
- Issue
- 4
- Pages
- 171-177
- ISSN
- 2452-3186 (ISSN-L)
- OpenAlex
- W2548247411
- Semantic Scholar
- e7bcd03bb8cee915b9f4370cb05d16dc21405b08
- Cited by
- 328
- References
- 161
- Citations by year
- 2026: 26 · 2025: 35 · 2024: 38 · 2023: 46 · 2022: 38 · 2021: 53 · 2020: 34 · 2019: 28 · 2018: 22 · 2017: 8
- FWCI
- 20.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Research in Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- National Institute on Aging
- Topics
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
- Keywords
- myofibroblasts, wound healing, chronic wounds, fibrosis, hypertrophic scars, extracellular matrix, tissue repair, myofibroblast activation, diabetes mellitus, therapeutic target
- MeSH terms
- Animals, Cicatrix, Contracture, Extracellular Matrix, Fibrosis, Granulation Tissue, Humans, Wound Healing, Apoptosis, Intercellular Signaling Peptides and Proteins, Myofibroblasts
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