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J Mol Cell Cardiol. 2016 Feb;91:114-22. doi: 10.1016/j.yjmcc.2015.12.024. Epub 2015 Dec 29.

The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction.

Author information

1
Department of Pharmacology, University of California Davis, School of Medicine, Davis, CA, USA.
2
Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center and Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS, USA.
3
Department of Pharmacology, University of California Davis, School of Medicine, Davis, CA, USA. Electronic address: cripplinger@ucdavis.edu.

Abstract

Optimal healing of damaged tissue following myocardial infarction (MI) requires a coordinated cellular response that can be divided into three phases: inflammatory, proliferative/reparative, and maturation. The inflammatory phase, characterized by rapid influx of cytokines, chemokines, and immune cells, is critical to the removal of damaged tissue. The onset of the proliferative/reparative phase is marked by increased proliferation of myofibroblasts and secretion of collagen to replace dead tissue. Lastly, crosslinking of collagen fibers and apoptosis of immune cells marks the maturation phase. Excessive inflammation or fibrosis has been linked to increased incidence of arrhythmia and other MI-related pathologies. This review describes the roles of inflammation and fibrosis in arrhythmogenesis and prospective therapies for anti-arrhythmic treatment.

KEYWORDS:

Arrhythmia; Fibrosis; Inflammation; Myocardial infarction

PMID:
26739214
PMCID:
PMC4764395
DOI:
10.1016/j.yjmcc.2015.12.024
[Indexed for MEDLINE]
Free PMC Article

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