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

Samantha D. Francis Stuart; Nicole M. De Jesus; Merry L. Lindsey; Crystal M. Ripplinger

doi:10.1016/j.yjmcc.2015.12.024

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

Samantha D. Francis Stuart, Nicole M. De Jesus, Merry L. Lindsey, Crystal M. Ripplinger

Research output: Contribution to journal › Review article › peer-review

93 Scopus citations

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.

Original language	English (US)
Pages (from-to)	114-122
Number of pages	9
Journal	Journal of Molecular and Cellular Cardiology
Volume	91
DOIs	https://doi.org/10.1016/j.yjmcc.2015.12.024
State	Published - Feb 1 2016
Externally published	Yes

Keywords

Arrhythmia
Fibrosis
Inflammation
Myocardial infarction

ASJC Scopus subject areas

Molecular Biology
Cardiology and Cardiovascular Medicine

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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",

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AU - Francis Stuart, Samantha D.

AU - De Jesus, Nicole M.

AU - Lindsey, Merry L.

AU - Ripplinger, Crystal M.

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N2 - 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.

AB - 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.

KW - Arrhythmia

KW - Fibrosis

KW - Inflammation

KW - Myocardial infarction

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