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

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...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2016-02, Vol.91, p.114-122
Main Authors: Francis Stuart, Samantha D, De Jesus, Nicole M, Lindsey, Merry L, Ripplinger, Crystal M
Format: Article
Language:English
Subjects:
Animals
Arrhythmia
Arrhythmias, Cardiac - complications
Arrhythmias, Cardiac - genetics
Arrhythmias, Cardiac - metabolism
Arrhythmias, Cardiac - pathology
Calcium - metabolism
Cardiovascular
Fibrosis
Gene Expression Regulation
Humans
Inflammation
Interleukin-1beta - genetics
Interleukin-1beta - metabolism
Interleukin-6 - genetics
Interleukin-6 - metabolism
Ion Transport
Matrix Metalloproteinases - genetics
Matrix Metalloproteinases - metabolism
Myocardial infarction
Myocardial Infarction - complications
Myocardial Infarction - genetics
Myocardial Infarction - metabolism
Myocardial Infarction - pathology
Myocardium - metabolism
Myocardium - pathology
Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics
Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism
Signal Transduction
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - metabolism
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Summary: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.
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2015.12.024