The Cardiomyocyte as a Source of Cytokines in Cardiac InjuryToshinori Aoyagi and Takashi Matsui*
Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813
- *Corresponding Author:
- Takashi Matsui, MD, PhD
Center for Cardiovascular Research
John A. Burns School of Medicine
University of Hawaii, 651 Ilalo St.
BSB#311D, Honolulu, HI 96813, USA
E-mail: [email protected]
Received date: November 01, 2011; Accepted date: December 13, 2011; Published date: December 15, 2011
Citation: Aoyagi T, Matsui T (2011) The Cardiomyocyte as a Source of Cytokines in Cardiac Injury. J Cell Sci Ther S5:003 doi: 10.4172/2157-7013.S5-003
Copyright: © 2011 Aoyagi T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Fibrosis induced by prolonged inflammation is a major pathophysiological feature of adverse left ventricular remodeling after myocardial infarction and pathological cardiac hypertrophy. Recent reports strongly suggest that the interaction between leukocytes, non-myocytes (mainly cardiac fibroblasts) and cardiomyocytes, possibly mediated by cytokine signaling, plays an important role in controlling the inflammatory reaction after cardiac injury. Therefore, controlling cytokine secretion from resident cardiomyocytes is one plausible strategy for preventing tissue damage.