Perspective Article: Tissue repair, contraction, and the myofibroblast

  title={Perspective Article: Tissue repair, contraction, and the myofibroblast},
  author={Alexis Desmouli{\`e}re and Christine Chaponnier and Giulio Gabbiani},
  journal={Wound Repair and Regeneration},
After the first description of the myofibroblast in granulation tissue of an open wound by means of electron microscopy, as an intermediate cell between the fibroblast and the smooth muscle cell, the myofibroblast has been identified both in normal tissues, particularly in locations where there is a necessity of mechanical force development, and in pathological tissues, in relation with hypertrophic scarring, fibromatoses and fibrocontractive diseases as well as in the stroma reaction to… 
Immunohistochemical and transmission electron microscopy study regarding myofibroblasts in fibroinflammatory epulis and giant cell peripheral granuloma.
The presence and distribution of myofibroblasts in the reactive stromal tissue of granulation tumors in the oral area, fibroinflammatory epulis and giant cells peripheral granuloma is emphasized by means of immunocytochemical and transmission electron microscopy studies.
Corneal myofibroblasts and fibrosis.
Angiogenic properties of myofibroblasts isolated from normal human skin wounds
It is hypothesized that normal wound myofibroblasts contribute to the vascular network development during wound healing and inhibition of TIMP-1 secretion using shRNA significantly decreased my ofibro Blasts induced angiogenesis.
Fibrosis and cancer: Do myofibroblasts come also from epithelial cells via EMT?
It is suggested that increased MMP expression may stimulate fibrosis, tumorigenesis, and tumor progression by inducing a specialized EMT in which epithelial cells transdifferentiate into activated myofibroblasts.
Hypoxia drives the transition of human dermal fibroblasts to a myofibroblast-like phenotype via the TGF-β1/Smad3 pathway
This study demonstrates for the first time that hypoxia facilitates the transition of dermal fibroblasts to myofibroblast through the activation of the TGF-β1/Smad3 signaling pathway and may provide a potential target for the treatment of keloids.
Transient expression of myofibroblast-like cells in rat rib fracture callus
The presence of myofibroblast-like cells in early rat rib callus indicates that in vivo contraction of early callus is a mechanism that may occur in fractures so as to facilitate healing, as it does in soft tissue wound repair.
Cellular and molecular pathology of HTS: basis for treatment
  • A. ArmourP. ScottE. Tredget
  • Biology, Medicine
    Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
  • 2007
The systemic response to injury appears to influence the local healing process whereby increases in Th2 and possibly Th3 cytokines such as IL‐2, IL‐4 and IL‐10 and TGF‐β are present in the circulating lymphocytes in these fibrotic conditions.
Connective tissue growth factor in tissue fibrosis
It is shown that CTGF plays a pivotal role in fibrosis and blocking CTGF activity may be useful as a specific target of attenuating fibrosis in SSc, and the reduction or absence of CTGF could abrogate fibrosis.
Review Article Multiple roles of a-smooth muscle actin in mechanotransduction
In addition to its importance as a structural protein in tissue remodeling and contraction, SMA may serve as a mechanotransducer, based on its ability to physically link mechanosensory elements and to enhance its own, force-induced expression.


The stroma reaction myofibroblast: a key player in the control of tumor cell behavior.
It is suggested that the myofibroblast may represent a new important target of antitumor therapy because of its ability to interact with epithelial cells and other connective tissue cells and may thus control such phenomena as tumor invasion and angiogenesis.
Alpha-smooth muscle actin is transiently expressed by myofibroblasts during experimental wound healing.
It is concluded that myofibroblasts develop gradually from granulation tissue fibroblast and temporarily express a marker of smooth muscle differentiation, which may be relevant for the understanding of the mechanisms of normal and pathologic wound healing.
Circulating fibrocytes: collagen-secreting cells of the peripheral blood.
Mechanical tension controls granulation tissue contractile activity and myofibroblast differentiation.
Transforming Growth Factor-ill Induces u-Smooth Muscle Actin Expression in Granulation Tissue Myofibroblasts and in Quiescent and Growing Cultured Fibroblasts
It is shown that the subcutaneous administration of transforming growth factor-ill to rats results in the formation of a granulation tissue in which a-SM actin expressing myofibroblasts are particularly abundant, and suggests that TGFfll plays an important role in my ofibroblast differentiation during wound healing and fibrocontractive diseases.
Normal skin wound and hypertrophic scar myofibroblasts have differential responses to apoptotic inductors
These results confirmed the hypothesis of defects in apoptosis and growth during pathological scar formation impeding myofibroblast disappearance at the end of healing and presented a broad vision of the apoptotic sensitivity of normal and pathological my ofibroblasts.
Circulating Fibrocytes Define a New Leukocyte Subpopulation That Mediates Tissue Repair
Blood-borne fibrocytes contribute to scar formation and may play an important role both in normal wound repair and in pathological fibrotic responses.
The Fibronectin Domain ED-A Is Crucial for Myofibroblastic Phenotype Induction by Transforming Growth Factor-β1
It is reported here that ED-A FN deposition precedes α-SM actin expression by fibroblasts during granulation tissue evolution in vivo and after TGFβ1 stimulation in vitro, and a hitherto unknown mechanism of cytokine-determined gene stimulation based on the generation of an ECM-derived permissive outside in signaling is identified.
Dissecting the roles of endothelin, TGF-beta and GM-CSF on myofibroblast differentiation by keratinocytes.
The results dissect the roles of TGF-beta and ET-1 on mechanical force generation in keratinocyte-fibroblast co-cultures, and identify GM-CSF as an inducer of myofibroblasts acting indirectly.