H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation
Author(s) -
Xiaohui Zhang,
Liya Pan,
Kelaier Yang,
Yu Fu,
Yue Liu,
Jinyu Chi,
Xin Zhang,
Siting Hong,
Xiao Ma,
Xinhua Yin
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000481843
Subject(s) - relaxin , diabetic cardiomyopathy , inflammasome , medicine , fibrosis , cardiac fibrosis , endocrinology , inflammation , streptozotocin , myocardial fibrosis , apoptosis , cardiac function curve , diabetes mellitus , cardiomyopathy , heart failure , biology , receptor , biochemistry
Apoptosis, fibrosis and NLRP3 inflammasome activation are involved in the development of diabetic cardiomyopathy (DCM). Human recombinant relaxin-3 (H3 relaxin) is a novel bioactive peptide that inhibits cardiac injury; however, whether H3 relaxin prevents cardiac injury in rats with DCM and the underlying mechanisms are unknown.
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