title: The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy.
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.
authors.affiliation: Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China. wangshudong816@163.com.
authors.forename: Shudong
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Radiation Oncology, the First Hospital of Jilin University, Changchun 130021, China. juanjuan1693@163.com.
authors.forename: Lijuan
authors.initials: L
authors.lastname: Ding
authors.affiliation: Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China. wsd816@163.com.
authors.forename: Honglei
authors.initials: H
authors.lastname: Ji
authors.affiliation: Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China. wsxuzheng@163.com.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Xu
authors.affiliation: Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China. liuquan@jlu.edu.cn.
authors.forename: Quan
authors.initials: Q
authors.lastname: Liu
authors.affiliation: Cardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China. zhengyang@jlu.edu.cn.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zheng
mesh_terms: D000818:Animals; D048909:Diabetes Complications / Q000517:prevention & control; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D058065:Diabetic Cardiomyopathies / Q000378:metabolism / Q000473:pathology*; D004734:Energy Metabolism; D035683:MicroRNAs / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D020033:Protein Isoforms / Q000037:antagonists & inhibitors / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D015398:Signal Transduction; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D035683:MicroRNAs; D020033:Protein Isoforms; D047428:Protein Kinase Inhibitors; D048051:p38 Mitogen-Activated Protein Kinases
keywords: cardiac dysfunction; diabetic cardiomyopathy; microRNAs; p38 MAPK