Mechanical tension controls granulation tissue contractile activity and myofibroblast differentiation.

By B. Hinz, D. Mastrangelo, C. Iselin, C. Chaponnier, G. Gabbiani. American Journal of Pathology, 2001

674 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Orthopedics and Sports Medicine

View Paper: https://www.semanticscholar.org/paper/85e8f0f877c08448b2d7b427ac5532c7702ecd80

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. B. Hinz
2. TA Wynn
3. S. Werner
4. Jeremy S. Duffield

In Neurology

1. B. Hinz
2. TA Wynn

In Orthopedics and Sports Medicine

1. B. Hinz
2. S. Werner
3. Nikolaos G. Frangogiannis

Citations in the corpus

• Fibroblasts and myofibroblasts in wound healing (2014, neutral): “However, some situations have been reported in the literature where myofibroblasts in some pathologies have been found to be desmin positive.(17) Distinguishing myofibroblasts from pericytes is perhaps more problematic since pericytes can closely resemble myofibroblasts in being α-SM actin positive,”
• The myofibroblast: paradigm for a mechanically active cell. (2010, background): “Concomitantly, myofibroblast differentiation and a-SMA expression on rigid plastic substrates or in mechanically stressed wounds are suppressed by inhibition of TGFb1 (Hinz et al., 2001a, 2001b).”
• Host Responses in Tissue Repair and Fibrosis (2012, background): “Indeed, there is growing recognition that biomechanical signaling, via tissue “stiffness,” is a pivotal mechanism for promoting and sustaining the differentiated, contractile myofibroblast phenotype (11, 12).”
• NADPH Oxidase-4 Mediates Myofibroblast Activation and Fibrogenic Responses to Lung Injury (2009, background): “Myofibroblast differentiation and activation are dependent on TGF-β1, matrix signaling and biomechanical tensio”
• Keratinocyte-fibroblast interactions in wound healing. (2007, background): “Several studies investigated the mechanisms on how fibroblasts become myofibroblasts, and it seems that the two most important stimuli are mechanical tension (Hinz et al., 2001) and TGF-b activity (Desmouliere et al.”
• Wound healing: cellular mechanisms and pathological outcomes (2020, background): “Heightened expression of TGF-β and mechanical tension stimulate myofibroblast differentiation in vivo and in vitro [93].”
• Myofibroblasts and mechano-regulation of connective tissue remodelling (2002, background): “Although tractional forces that are generated by fibroblasts might be sufficient to initiate wound closure, the subsequent appearance of resistance in the surrounding tissue induces the DIFFERENTIATION of myofibroblast”
• Formation and function of the myofibroblast during tissue repair. (2007, background): “These in vivo stress fibers are first composed of cytoplasmic actins and generate comparably small traction forces (Hinz et al., 2001b).”
• Cell Responses to Surface and Architecture of Tissue Engineering Scaffolds (2011, positive): “Tock et al (Tock et al., 2003) reported that mechanical loading impressed α -SMA expression, a marker of myofibroblasts hat mechanical tension in granulation tissues controls myofibroblast differentiation (Hinz et al., 2001).”
• Perspective Article: Tissue repair, contraction, and the myofibroblast (2005, background): “Recently, it has been shown that a-SMA participates importantly in force production by the myofibroblast both in vitro, using models involving fibroblasts cultured on flexible substrates or within floating and attached collagen gels,(11) and in vivo, using experimental wound healing in the rat.(12) ”