Role of interleukin-6 in Regulation of Immune Responses to Remodeling After Myocardial Infarction

Heart Fail Rev. 2015 Jan;20(1):25-38. doi: 10.1007/s10741-014-9431-1.


Myocardial remodeling following myocardial infarction (MI) is emerging as key causes of chronic infarct mortality. Interleukin-6 is a classic pro-inflammatory cytokine needed to mount an effective immune response. It seems that interleukin-6 acts as an important role in the dynamic and superbly orchestrated process of innate immunity after MI. Interleukin-6 timely suppresses of innate immune signals to prevent the catastrophic consequences of uncontrolled inflammation on cardiac geometry and function, and thus tunes myocardial remodeling. A comprehensive understanding of biological processes of interleukin-6 in innate immunity leading to inflammatory response and disease-related ventricular remodeling is helpful to find the solution of chronic heart failure. To accomplish this, we reviewed the articles of interleukin-6 regard to inflammation, innate immunity, and cardiac remodeling. This review focuses on the role of interleukin-6 that dominates cell-mediated immunity, especially on neutrophils, monocytes, macrophages, and fibroblasts. In addition, we will also briefly discuss other inflammatory cytokines involved in this process within the paper.

Publication types

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

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / immunology
  • Dendritic Cells / immunology
  • Fibroblasts / immunology
  • Heart Failure / physiopathology*
  • Humans
  • Immunity, Cellular
  • Immunity, Innate
  • Inflammation / immunology
  • Interleukin-6 / immunology*
  • Macrophages / immunology
  • Mice
  • Mice, Knockout
  • Monocytes / immunology
  • Myocardial Infarction / immunology
  • Myocardial Infarction / physiopathology*
  • Myocardium / immunology*
  • Neutrophils / immunology
  • Ventricular Remodeling / physiology*


  • Interleukin-6