Myocardial fibrosis seen through the lenses of T-cell biology

J Mol Cell Cardiol. 2016 Mar:92:41-5. doi: 10.1016/j.yjmcc.2016.01.018. Epub 2016 Jan 22.

Abstract

Lymphocytes came recently into focus as modulators of non-infectious myocardial diseases. Several lines of experimental evidence now indicate that CD4(+) T-cells can influence the healing and scarring processes that follow a myocardial infarction episode. Furthermore, such heart-directed T-cell activity has also been implicated in the pathogenesis cardiac remodeling that develops in response to chronic pressure-overload conditions. Mechanistically, different T-cell subsets can secrete several mediators and growth factors that influence the myocardial molecular milieu and directly interfere with the macrophages' and fibroblasts' activity. Therefore, the present review summarizes the current experimental evidence on the role of T-cells in myocardial scar formation after infarction and myocardial fibrosis as central mechanism of ventricular remodeling.

Keywords: Healing; Myocardial fibrosis; Myocardial infarction; T-cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / metabolism*
  • CD4-Positive T-Lymphocytes / pathology
  • Cardiomyopathies / immunology
  • Cardiomyopathies / metabolism*
  • Cardiomyopathies / pathology
  • Humans
  • Macrophages / metabolism
  • Macrophages / pathology
  • Myocardial Infarction / immunology
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Myocardium / metabolism
  • Myocardium / pathology
  • T-Lymphocyte Subsets / metabolism*
  • T-Lymphocyte Subsets / pathology
  • Ventricular Remodeling / immunology
  • Wound Healing / immunology