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dc.contributor.authorMigneault, Francis
dc.contributor.authorHébert, Marie-Josée
dc.date.accessioned2021-01-15T13:33:26Z
dc.date.availableMONTHS_WITHHELD:12fr
dc.date.available2021-01-15T13:33:26Z
dc.date.issued2021-01-14
dc.identifier.urihttp://hdl.handle.net/1866/24245
dc.publisherElsevierfr
dc.titleAutophagy, tissue repair, and fibrosis: a delicate balancefr
dc.typeArticlefr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de médecinefr
dc.identifier.doi10.1016/j.matbio.2021.01.003
dcterms.abstractTissue repair and fibrosis, an abnormal form of repair, occur in most human organs in response to injury or inflammation. Fibroblasts play a major role in the normal repair process by differentiating into myofibroblasts that synthesize extracellular matrix (ECM) components and favor tissue remodeling to reestablish normal function and integrity. However, their persistent accumulation at the site of injury is a hallmark of fibrosis. Autophagy is a catabolic process that occurs in eukaryotic cells as a stress response to allow cell survival and maintenance of cellular homeostasis by degrading and recycling intracellular components. Recent advances identify autophagy as an important regulator of myofibroblast differentiation, tissue remodeling, and fibrogenesis. In this mini-review, we provide an overview of the interactions between autophagy, ECM, and fibrosis, and emphasize the molecular mechanisms involved in myofibroblast differentiation. We also describe the emerging concept of secretory autophagy as a new avenue for intercellular communication at the site of tissue injury and repair.fr
dcterms.isPartOfurn:ISSN:0945-053Xfr
dcterms.languageengfr
UdeM.ReferenceFournieParDeposanthttps://doi.org/10.1016/j.matbio.2021.01.003fr
UdeM.VersionRioxxVersion acceptée / Accepted Manuscriptfr
oaire.citationTitleMatrix biologyfr


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