Mechanosensing and fibrosis
Daniel J. Tschumperlin,1 Giovanni Ligresti,1 Moira B. Hilscher,2 and Vijay H. Shah2
1Department of Physiology and Biomedical Engineering and
2Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Address correspondence to: Daniel J. Tschumperlin, Mayo Clinic, Department of Physiology and Biomedical Engineering, 200 First Street SW, Rochester, Minnesota 55905, USA. Phone: 507.255.8475; E-mail: Tschumperlin.Daniel@mayo.edu.
Find articles by Tschumperlin, D. in: JCI | PubMed | Google Scholar
1Department of Physiology and Biomedical Engineering and
2Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Address correspondence to: Daniel J. Tschumperlin, Mayo Clinic, Department of Physiology and Biomedical Engineering, 200 First Street SW, Rochester, Minnesota 55905, USA. Phone: 507.255.8475; E-mail: Tschumperlin.Daniel@mayo.edu.
Find articles by Ligresti, G. in: JCI | PubMed | Google Scholar
1Department of Physiology and Biomedical Engineering and
2Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Address correspondence to: Daniel J. Tschumperlin, Mayo Clinic, Department of Physiology and Biomedical Engineering, 200 First Street SW, Rochester, Minnesota 55905, USA. Phone: 507.255.8475; E-mail: Tschumperlin.Daniel@mayo.edu.
Find articles by Hilscher, M. in: JCI | PubMed | Google Scholar
1Department of Physiology and Biomedical Engineering and
2Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Address correspondence to: Daniel J. Tschumperlin, Mayo Clinic, Department of Physiology and Biomedical Engineering, 200 First Street SW, Rochester, Minnesota 55905, USA. Phone: 507.255.8475; E-mail: Tschumperlin.Daniel@mayo.edu.
Find articles by Shah, V. in: JCI | PubMed | Google Scholar
First published January 2, 2018 - More info
J Clin Invest. 2018;128(1):74–84. https://doi.org/10.1172/JCI93561.
Copyright © 2018, American Society for Clinical Investigation
Tissue injury disrupts the mechanical homeostasis that underlies normal tissue architecture and function. The failure to resolve injury and restore homeostasis gives rise to progressive fibrosis that is accompanied by persistent alterations in the mechanical environment as a consequence of pathological matrix deposition and stiffening. This Review focuses on our rapidly growing understanding of the molecular mechanisms linking the altered mechanical environment in injury, repair, and fibrosis to cellular activation. In particular, our focus is on the mechanisms by which cells transduce mechanical signals, leading to transcriptional and epigenetic responses that underlie both transient and persistent alterations in cell state that contribute to fibrosis. Translation of these mechanobiological insights may enable new approaches to promote tissue repair and arrest or reverse fibrotic tissue remodeling.
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