Fibroblast and myofibroblast activation in normal tissue repair and fibrosis.

Autor: Younesi FS; Keenan Research Institute for Biomedical Science of the St. Michael's Hospital, Toronto, Ontario, Canada.; Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada., Miller AE; Department of Biomedical Engineering, School of Engineering and Applied Science, University of Virginia, Charlottesville, VA, USA., Barker TH; Department of Biomedical Engineering, School of Engineering and Applied Science, University of Virginia, Charlottesville, VA, USA., Rossi FMV; School of Biomedical Engineering and Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada., Hinz B; Keenan Research Institute for Biomedical Science of the St. Michael's Hospital, Toronto, Ontario, Canada. boris.hinz@utoronto.ca.; Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada. boris.hinz@utoronto.ca.
Jazyk: angličtina
Zdroj: Nature reviews. Molecular cell biology [Nat Rev Mol Cell Biol] 2024 Aug; Vol. 25 (8), pp. 617-638. Date of Electronic Publication: 2024 Apr 08.
DOI: 10.1038/s41580-024-00716-0
Abstrakt: The term 'fibroblast' often serves as a catch-all for a diverse array of mesenchymal cells, including perivascular cells, stromal progenitor cells and bona fide fibroblasts. Although phenotypically similar, these subpopulations are functionally distinct, maintaining tissue integrity and serving as local progenitor reservoirs. In response to tissue injury, these cells undergo a dynamic fibroblast-myofibroblast transition, marked by extracellular matrix secretion and contraction of actomyosin-based stress fibres. Importantly, whereas transient activation into myofibroblasts aids in tissue repair, persistent activation triggers pathological fibrosis. In this Review, we discuss the roles of mechanical cues, such as tissue stiffness and strain, alongside cell signalling pathways and extracellular matrix ligands in modulating myofibroblast activation and survival. We also highlight the role of epigenetic modifications and myofibroblast memory in physiological and pathological processes. Finally, we discuss potential strategies for therapeutically interfering with these factors and the associated signal transduction pathways to improve the outcome of dysregulated healing.
(© 2024. Springer Nature Limited.)
Databáze: MEDLINE
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