
The Opening of ATP-Sensitive K+ Channels Protects H9c2 Cardiac Cells Against the High Glucose-Induced Injury and Inflammation by Inhibiting the ROS-TLR4-Necroptosis Pathway
Author(s) -
Weijie Liang,
Meiji Chen,
Duo Zheng,
Li Jianhao,
Mingke Song,
Wenzhu Zhang,
Jianqiang Feng,
Jun Liu
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 - 10.1159/000461391
Subject(s) - inflammation , necroptosis , tlr4 , microbiology and biotechnology , chemistry , signal transduction , pharmacology , apoptosis , programmed cell death , medicine , biology , biochemistry , immunology
Hyperglycemia activates multiple signaling molecules, including reactive oxygen species (ROS), toll-like receptor 4 (TLR4), receptor-interacting protein 3 (RIP3, a kinase promoting necroptosis), which mediate hyperglycemia-induced cardiac injury. This study explored whether inhibition of ROS-TLR4-necroptosis pathway contributed to the protection of ATP-sensitive K+ (KATP) channel opening against high glucose-induced cardiac injury and inflammation.