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Cited by 1,039Wound Healing and TreatmentsDermatologic Treatments and ResearchLiver physiology and pathology

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Fibroblasts and myofibroblasts in wound healing

Open access
Desmouliere, Alexis, Darby, Ian Andrew, Laverdet, Betty, Bonté, Frédéric·2014·Clinical, Cosmetic and Investigational Dermatology
DOI 10.2147/ccid.s50046PMC PMC4226391
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Abstract

(Myo)fibroblasts are key players for maintaining skin homeostasis and for orchestrating physiological tissue repair. (Myo)fibroblasts are embedded in a sophisticated extracellular matrix (ECM) that they secrete, and a complex and interactive dialogue exists between (myo)fibroblasts and their microenvironment. In addition to the secretion of the ECM, (myo)fibroblasts, by secreting matrix metalloproteinases and tissue inhibitors of metalloproteinases, are able to remodel this ECM. (Myo)fibroblasts and their microenvironment form an evolving network during tissue repair, with reciprocal actions leading to cell differentiation, proliferation, quiescence, or apoptosis, and actions on growth factor bioavailability by binding, sequestration, and activation. In addition, the (myo)fibroblast phenotype is regulated by mechanical stresses to which they are subjected and thus by mechanical signaling. In pathological situations (excessive scarring or fibrosis), or during aging, this dialogue between the (myo)fibroblasts and their microenvironment may be altered or disrupted, leading to repair defects or to injuries with damaged and/or cosmetic skin alterations such as wrinkle development. The intimate dialogue between the (myo)fibroblasts and their microenvironment therefore represents a fascinating domain that must be better understood in order not only to characterize new therapeutic targets and drugs able to prevent or treat pathological developments but also to interfere with skin alterations observed during normal aging or premature aging induced by a deleterious environment.

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Figure 1 The various phases of the healing process. Notes: After damage, inflammation leads to the formation of the granulation tissue, during which myofibroblasts appear. An important neoangiogenesis is also observed. On this granulation tissue, a new epidermis can then develop. Subsequently, remodeling of this granulation tissue occurs with apoptosis of the cells present in the granulation tissue (myofibroblasts and vascular cells) and reorganization of the extracellular matrix.
Figure 1 The various phases of the healing process. Notes: After damage, inflammation leads to the formation of the granulation tissue, during which myofibroblasts appear. An important neoangiogenesis is also observed. On this granulation tissue, a new epidermis can then develop. Subsequently, remodeling of this granulation tissue occurs with apoptosis of the cells present in the granulation tissue (myofibroblasts and vascular cells) and reorganization of the extracellular matrix.CC BY-NC · PubMed Central
Figure 2 Schematic illustration showing the evolution of the (myo)fibroblast phenotype. Notes: The myofibroblastic modulation of fibroblastic cells begins with the appearance of the proto myofibroblast, whose stress fibers contain only β- and γ-cytoplasmic actins and evolves, but not necessarily always, into the appearance of the differentiated myofibroblast, the most common variant of this cell, with stress fibers containing α-smooth muscle actin. Soluble factors, extracellular matrix components, and/or the mechanical microenvironment are involved in myofibroblastic differentiation. The myofibroblast can disappear by apoptosis; while deactivation leading to a quiescent phenotype has not been clearly demonstrated, at least in vivo.
Figure 2 Schematic illustration showing the evolution of the (myo)fibroblast phenotype. Notes: The myofibroblastic modulation of fibroblastic cells begins with the appearance of the proto myofibroblast, whose stress fibers contain only β- and γ-cytoplasmic actins and evolves, but not necessarily always, into the appearance of the differentiated myofibroblast, the most common variant of this cell, with stress fibers containing α-smooth muscle actin. Soluble factors, extracellular matrix components, and/or the mechanical microenvironment are involved in myofibroblastic differentiation. The myofibroblast can disappear by apoptosis; while deactivation leading to a quiescent phenotype has not been clearly demonstrated, at least in vivo.CC BY-NC · PubMed Central
Figure 3 Pathological situations. Notes: If the inflammation phase persists and the granulation tissue does not develop, a chronic wound may result. If the remodeling phase of the granulation tissue does not happen (neither apoptosis of the cells present in the granulation tissue, myofibroblasts, and vascular cells, nor reorganization of the extracellular matrix), myofibroblasts may persist, leading to pathological situations characterized by excessive scarring.
Figure 3 Pathological situations. Notes: If the inflammation phase persists and the granulation tissue does not develop, a chronic wound may result. If the remodeling phase of the granulation tissue does not happen (neither apoptosis of the cells present in the granulation tissue, myofibroblasts, and vascular cells, nor reorganization of the extracellular matrix), myofibroblasts may persist, leading to pathological situations characterized by excessive scarring.CC BY-NC · PubMed Central
Figure 4 Processes leading to normal wound repair and pathological scarring. Notes: In all of these situations, interactions between fibroblasts/myofibroblasts and the extracellular matrix, and also epithelial–mesenchymal cell dialogue, play a major role.
Figure 4 Processes leading to normal wound repair and pathological scarring. Notes: In all of these situations, interactions between fibroblasts/myofibroblasts and the extracellular matrix, and also epithelial–mesenchymal cell dialogue, play a major role.CC BY-NC · PubMed Central
Figure 5 The interactions between the dermis and the epidermis. Notes: The dermis and the epidermis contain nerves, but only the dermis is vascularized. The epidermis thus derives all its nutrients from dermal vessels (arrows). The dermal–epidermal junction plays a major role in the intense dialogue that exists between the keratinocytes of the epidermis and the cells of the dermis, notably the fibroblasts.
Figure 5 The interactions between the dermis and the epidermis. Notes: The dermis and the epidermis contain nerves, but only the dermis is vascularized. The epidermis thus derives all its nutrients from dermal vessels (arrows). The dermal–epidermal junction plays a major role in the intense dialogue that exists between the keratinocytes of the epidermis and the cells of the dermis, notably the fibroblasts.CC BY-NC · PubMed Central

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Metadata

Authors
Desmouliere, A., Darby, I. A., Laverdet, B., & Bonté, F.
Affiliations
  • RMIT University (AU)
  • Université de Limoges (FR)
  • LVMH (France) (FR)
ORCID
Venue
Clinical, Cosmetic and Investigational Dermatology
Publisher
Informa UK Limited
Published
2014-11
Volume
7
Pages
301
ISSN
1178-7015 (ISSN-L)
DOI
10.2147/ccid.s50046
PMC
PMC4226391
OpenAlex
W2023805473
Cited by
1,039
References
76
Citations by year
2026: 43 · 2025: 98 · 2024: 103 · 2023: 115 · 2022: 121 · 2021: 123 · 2020: 117 · 2019: 108 · 2018: 91 · 2017: 61 · 2016: 37 · 2015: 21
FWCI
4.89
Type
journal article
Language
en
Open access
Licence
Locations
  • Clinical Cosmetic and Investigational Dermatology (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • RMIT Research Repository (RMIT University Library) (submittedVersion)
  • Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
  • Figshare (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Wound Healing and Treatments
  • Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
fibroblasts, myofibroblasts, wound healing, skin homeostasis, extracellular matrix, matrix metalloproteinases, tissue inhibitors of metalloproteinases, extracellular matrix remodeling, growth factor bioavailability, mechanical signaling, fibrosis, scar formation, skin aging, wrinkle formation, cell-microenvironment interactions

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