Next Article in Journal
Prognostic Value of Affective Symptoms in First-Admission Psychotic Patients
Next Article in Special Issue
Anti-Diabetic Effect of Portulaca oleracea L. Polysaccharideandits Mechanism in Diabetic Rats
Previous Article in Journal
A WDR Gene Is a Conserved Member of a Chitin Synthase Gene Cluster and Influences the Cell Wall in Aspergillus nidulans
Previous Article in Special Issue
Computational Analysis of Single Nucleotide Polymorphisms Associated with Altered Drug Responsiveness in Type 2 Diabetes
Article Menu
Issue 7 (July) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2016, 17(7), 1037;

The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy

Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China
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)
Full-Text   |   PDF [509 KB, uploaded 30 June 2016]   |  


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

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Share & Cite This Article

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.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top