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 GePublished 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
- liver failure
- oxidative stress
- respiratory failure
- mild cognitive impairment
- ischemia reperfusion injury
- drug induced
- intensive care unit
- metabolic syndrome
- brain injury
- wound healing
- insulin resistance
- soft tissue
- blood brain barrier
- weight loss
- extracorporeal membrane oxygenation