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The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias.

Author information

1
Department of Molecular Biophysics and Physiology, Rush University Medical Center, 1750 W Harrison St, Chicago, IL, 60612, USA. xun_ai@rush.edu.
2
Department of Molecular Biophysics and Physiology, Rush University Medical Center, 1750 W Harrison St, Chicago, IL, 60612, USA.

Abstract

Stress-response kinases, the mitogen-activated protein kinases (MAPKs) are activated in response to the challenge of a myriad of stressors. c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinases (ERKs), and p38 MAPKs are the predominant members of the MAPK family in the heart. Extensive studies have revealed critical roles of activated MAPKs in the processes of cardiac injury and heart failure and many other cardiovascular diseases. Recently, emerging evidence suggests that MAPKs also promote the development of cardiac arrhythmias. Thus, understanding the functional impact of MAPKs in the heart could shed new light on the development of novel therapeutic approaches to improve cardiac function and prevent arrhythmia development in the patients. This review will summarize the recent findings on the role of MAPKs in cardiac remodeling and arrhythmia development and point to the critical need of future studies to further elucidate the fundamental mechanisms of MAPK activation and arrhythmia development in the heart.

KEYWORDS:

Aging; Arrhythmia; Cardiovascular diseases; Heart; Mitogen-activated protein kinases; Stress

PMID:
27848025
DOI:
10.1007/112_2016_8
[Indexed for MEDLINE]

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