TY - JOUR
T1 - The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction
AU - Francis Stuart, Samantha D.
AU - De Jesus, Nicole M.
AU - Lindsey, Merry L.
AU - Ripplinger, Crystal M.
N1 - Funding Information:
This work was supported by the National Institutes of Health HL075360 and GM114833 (to MLL) and HL111600 (to CMR), the American Heart Association 12SDG9010015 (to CMR), and the Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award 5I01BX000505 (to MLL).
Publisher Copyright:
© 2015 Elsevier Ltd.
PY - 2016/2/1
Y1 - 2016/2/1
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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U2 - 10.1016/j.yjmcc.2015.12.024
DO - 10.1016/j.yjmcc.2015.12.024
M3 - Review article
C2 - 26739214
AN - SCOPUS:84953313607
VL - 91
SP - 114
EP - 122
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
SN - 0022-2828
ER -