Exogenous Hydrogen Sulfide Attenuates Cardiac Fibrosis Through Reactive Oxygen Species Signal Pathways in Experimental Diabetes Mellitus Models
Author(s) -
Dan Zheng,
Shiyun Dong,
Ting Li,
Fan Yang,
Xiangjing Yu,
Jichao Wu,
Xin Zhong,
Yajun Zhao,
Lina Wang,
Changqing Xu,
Fanghao Lu,
Weihua Zhang
Publication year - 2015
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 - 10.1159/000430266
Subject(s) - nox4 , diabetic cardiomyopathy , cardiac fibrosis , myocardial fibrosis , nadph oxidase , reactive oxygen species , oxidative stress , fibrosis , cystathionine beta synthase , medicine , endocrinology , cardiomyopathy , streptozotocin , chemistry , diabetes mellitus , biochemistry , heart failure , enzyme , cysteine
Oxidative stress inducing hyperglycemia and high glucose play an important role in the development of cardiac fibrosis associated with diabetic cardiomyopathy. The endogenous gasotransmitter hydrogen sulfide (H2S) can act in a cytoprotective manner. However, whether H2S could inhibit the fibrotic process is unclear. The purpose of our study was to examine the role of H2S in the development and underlying mechanisms behind diabetic cardiomyopathy.
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