Cited by 328Wound Healing and TreatmentsLiver physiology and pathologyDermatologic Treatments and Research

The role of myofibroblasts in wound healing

Hinz, B.·2016·Current Research in Translational Medicine

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.

Integrity signals

Registry

Crossref · 10.1016/j.retram.2016.09.003

Cites

160 of 160 references verified0 citation errors · 0 not checkable

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  • Myofibroblast-induced fibrosis can be over-activated by Th2-derived cytokines IL-4 and IL-13.

    “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]

  • Th1 cytokines, such as IFN-γ, attenuate excessive scar formation.

    “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]

  • Myofibroblast-induced fibrosis can be over-activated by signaling through TGF-β.

    “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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Authors
Hinz, B.
Affiliations
University of Toronto (CA)
Corresponding author
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
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 › Rehabilitation › 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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