Augmentation of Histone Deacetylase 6 Activity Impairs Mitochondrial Respiratory Complex I in Ischemic/Reperfused Diabetic Hearts.

Shelley L BaumgardtJuan FangXuebin FuYanan LiuZhengyuan XiaMing ZhaoLing ChenRachana MishraMuthukumar GunasekaranProgyaparamita SahaJoseph M ForbessZeljko J BosnjakAmadou Ks CamaraJudy R KerstenEdward Benjamin ThorpSunjay KaushalZhi-Dong Ge

Published in: bioRxiv : the preprint server for biology (2023)

, implying that HDAC6 knockdown can preserve mCI activity in high glucose and hypoxia/reoxygenation. These results demonstrate that HDAC6 is an important mediator in MIRI and cardiac function in diabetes. Selective inhibition of HDAC6 has high therapeutic potential for acute IHS in diabetes.

Keyphrases

histone deacetylase
type diabetes
high glucose
endothelial cells
cardiovascular disease
glycemic control
oxidative stress
liver failure
induced apoptosis
ischemia reperfusion injury
drug induced
aortic dissection
wound healing
cerebral ischemia
endoplasmic reticulum stress
mechanical ventilation