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Role of interleukin-6 in regulation of immune responses to remodeling after myocardial infarction.

Abstract
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.
AuthorsMingyuan Huang, Du Yang, Meixiang Xiang, Jianan Wang
JournalHeart failure reviews (Heart Fail Rev) Vol. 20 Issue 1 Pg. 25-38 (Jan 2015) ISSN: 1573-7322 [Electronic] United States
PMID24756455 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Interleukin-6
Topics
  • 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, physiopathology)
  • Myocardium (immunology)
  • Neutrophils (immunology)
  • Ventricular Remodeling (physiology)

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