Dexmedetomidine protects H9c2 cardiomyocytes against oxygen-glucose deprivation/reoxygenation-induced intracellular calcium overload and apoptosis through regulating FKBP12.6/RyR2 signaling.

Mei YuanXiao-Wen MengJiao MaHong LiuShao-Yong SongQing-Cai ChenHua-Yue LiuJuan ZhangNan SongFu-Hai JiKe Peng

Published in: Drug design, development and therapy (2019)

This study indicates that DEX pretreatment protects the cardiomyocytes against OGD/R-induced injury by inhibiting [Ca2+]i overload and cell apoptosis via regulating the FKBP12.6/RyR2 signaling. DEX may be used for preventing cardiac I/R injury in the clinical settings.

Keyphrases

high glucose
diabetic rats
endothelial cells
oxidative stress
signaling pathway
cell proliferation
endoplasmic reticulum stress
drug induced
heart failure
induced apoptosis
left ventricular
metabolic syndrome
cell cycle arrest