The paradoxical role of inflammation in cardiac repair and regeneration - PubMed (original) (raw)
Review
The paradoxical role of inflammation in cardiac repair and regeneration
Bingbing Jiang et al. J Cardiovasc Transl Res. 2010 Aug.
Abstract
Inflammation has emerged as a critical biological process contributing to nearly all aspects of cardiovascular diseases including heart failure. Heart failure represents the final consequence of a diverse set of initial insults to the myocardium, among which myocardial infarction (MI) is the most common cause. After MI, the lack of perfusion often leads to the death of cardiomyocytes. The necrotic cells trigger a cascade of inflammatory pathways that work to clear the dead cells and matrix debris, as well as to repair and heal damaged tissues. For the heart, an organ with limited regeneration capacity, the consequence of MI (termed post-MI remodeling) comprises a series of structural and functional changes, including scar formation at the infarct zone, reactive hypertrophy of the remaining cardiomyocytes at the noninfarct area, ventricular chamber dilatation, and molecular changes marked by fetal gene up-regulation, all of which have been linked to the activation of the inflammatory pathways. Inadequate or excessive inflammatory response may lead to improper cellular repair, tissue damage, and dysfunction. Herein, we summarize the current understanding of the role of inflammation in cardiac injury and repair and put forth the hypothesis that temporally regulated activation and suppression of inflammation may be critical for achieving effective cardiac repair and regeneration.
References
- Nat Med. 2009 Dec;15(12):1363-4 - PubMed
- Am J Respir Cell Mol Biol. 2007 Jul;37(1):38-47 - PubMed
- Circulation. 1998 Apr 14;97(14):1382-91 - PubMed
- Cell. 2009 Jun 12;137(6):1112-23 - PubMed
- Br J Pharmacol. 2000 Oct;131(3):415-22 - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources