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Int. J. Mol. Sci. 2016, 17(7), 1037; doi:10.3390/ijms17071037

The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy

1
Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China
2
Department of Radiation Oncology, the First Hospital of Jilin University, Changchun 130021, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Lu Cai
Received: 30 May 2016 / Revised: 20 June 2016 / Accepted: 24 June 2016 / Published: 30 June 2016
(This article belongs to the Special Issue Diabetic Complications: Pathophysiology, Mechanisms, and Therapies)
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Abstract

Diabetic cardiomyopathy (DCM) is a major complication of diabetes that contributes to an increase in mortality. A number of mechanisms potentially explain the development of DCM including oxidative stress, inflammation and extracellular fibrosis. Mitogen-activated protein kinase (MAPK)-mediated signaling pathways are common among these pathogenic responses. Among the diverse array of kinases, extensive attention has been given to p38 MAPK due to its capacity for promoting or inhibiting the translation of target genes. Growing evidence has indicated that p38 MAPK is aberrantly expressed in the cardiovascular system, including the heart, under both experimental and clinical diabetic conditions and, furthermore, inhibition of p38 MAPK activation in transgenic animal model or with its pharmacologic inhibitor significantly prevents the development of DCM, implicating p38 MAPK as a novel diagnostic indicator and therapeutic target for DCM. This review summarizes our current knowledge base to provide an overview of the impact of p38 MAPK signaling in diabetes-induced cardiac remodeling and dysfunction. View Full-Text
Keywords: diabetic cardiomyopathy; p38 MAPK; cardiac dysfunction; microRNAs diabetic cardiomyopathy; p38 MAPK; cardiac dysfunction; microRNAs
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MDPI and ACS Style

Wang, S.; Ding, L.; Ji, H.; Xu, Z.; Liu, Q.; Zheng, Y. The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy. Int. J. Mol. Sci. 2016, 17, 1037.

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