Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart

Aude Angelini, Jo Ann Trial, Jesus Ortiz-Urbina, Katarzyna A. Cieslik

Research output: Contribution to journalReview articlepeer-review

42 Scopus citations

Abstract

The myofibroblast is a specialized fibroblast that expresses α-smooth muscle actin (α-SMA) and participates in wound contraction and fibrosis. The fibroblast to myofibroblast transition depends on chemical and mechanical signals. A fibroblast senses the changes in the environment (extracellular matrix (ECM)) and transduces these changes to the cytoskeleton and the nucleus, resulting in activation or inhibition of α-SMA transcription in a process called mechanosensing. A stiff matrix greatly facilitates the transition from fibroblast to myofibroblast, and although the aging heart is much stiffer than the young one, the aging fibroblast has difficulties in transitioning into the contractile phenotype. This suggests that the events occurring downstream of the matrix, such as activation or changes in expression levels of various proteins participating in mechanotransduction can negatively alter the ability of the aging fibroblast to become a myofibroblast. In this review, we will discuss in detail the changes in ECM, receptors (integrin or non-integrin), focal adhesions, cytoskeleton, and transcription factors involved in mechanosensing that occur with aging.

Original languageEnglish (US)
Article number101150
JournalAgeing Research Reviews
Volume63
DOIs
StatePublished - Nov 2020

Keywords

  • Aging
  • Cardiac fibroblast
  • Mechanosensing
  • Myofibroblast

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Aging
  • Molecular Biology
  • Neurology

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