title: Molecular networks underlying myofibroblast fate and fibrosis.
abstract: Fibrotic remodeling is a hallmark of most forms of cardiovascular disease and a strong prognostic indicator of the advancement towards heart failure. Myofibroblasts, which are a heterogeneous cell-type specialized for extracellular matrix (ECM) secretion and tissue contraction, are the primary effectors of the heart's fibrotic response. This review is focused on defining myofibroblast physiology, its progenitor cell populations, and the core signaling network that orchestrates myofibroblast differentiation as a way of understanding the basic determinants of fibrotic disease in the heart and other tissues.
authors.affiliation: Division of Cardiology, University of Washington School of Medicine, Seattle, WA, USA.
authors.forename: April
authors.initials: A
authors.lastname: Stempien-Otero
authors.affiliation: Department of Bioengineering, University of Washington, Seattle, WA, USA.
authors.forename: Deok-Ho
authors.initials: DH
authors.lastname: Kim
authors.affiliation: Department of Pathology, University of Washington School of Medicine, Seattle, WA, USA; Department of Bioengineering, University of Washington, Seattle, WA, USA. Electronic address: jendavis@uw.edu.
authors.forename: Jennifer
authors.initials: J
authors.lastname: Davis
mesh_terms: D000818:Animals; D015415:Biomarkers; D002454:Cell Differentiation; D005355:Fibrosis; D005786:Gene Expression Regulation; D053263:Gene Regulatory Networks; D006801:Humans; D058628:Myofibroblasts / Q000166:cytology* / Q000502:physiology*; D010641:Phenotype; D015398:Signal Transduction
chemical_list: D015415:Biomarkers
keywords: Actin cytoskeleton; Differentiation; Fibrosis; Mitogen activated protein kinases; Myofibroblast; RNA binding proteins; TGFβ; TRP channels