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 kinase (ERK), and MAPK p38 are the important members of the MAPK family in the heart. Extensive studies have revealed critical roles of activated MAPKs in the processes of cardiac injury, cardiac arrhythmias, heart failure, and other cardiovascular diseases. Advancing our understanding regarding the functional impacts of MAPKs in the development of heart diseases could shed new light on developing novel therapeutic approaches to improve cardiac function and prevent arrhythmia development in patients. This chapter summarizes relevant current knowledge on the pivotal roles of MAPKs in physiopathological and molecular remodeling in cardiac myocytes during the disease development and for the therapeutic potentials of developing MAPK inhibitors and/or activators.
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