Molecular networks underlying myofibroblast fate and fibrosis

J Mol Cell Cardiol. 2016 Aug:97:153-61. doi: 10.1016/j.yjmcc.2016.05.002. Epub 2016 May 7.

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.

Keywords: Actin cytoskeleton; Differentiation; Fibrosis; Mitogen activated protein kinases; Myofibroblast; RNA binding proteins; TGFβ; TRP channels.

Publication types

  • Review
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Biomarkers
  • Cell Differentiation
  • Fibrosis
  • Gene Expression Regulation*
  • Gene Regulatory Networks*
  • Humans
  • Myofibroblasts / cytology*
  • Myofibroblasts / physiology*
  • Phenotype
  • Signal Transduction*

Substances

  • Biomarkers