Akap1 deficiency exacerbates diabetic cardiomyopathy in mice by NDUFS1-mediated mitochondrial dysfunction and apoptosis.
Bingchao QiLinjie HeYa ZhaoLing ZhangYuanfang HeJun LiCongye LiBo ZhangQichao HuangJinliang XingFei LiYan LiJoris HoeksPublished in: Diabetologia (2020)
Our study provides the first evidence that Akap1 deficiency exacerbates diabetic cardiomyopathy by impeding mitochondrial translocation of NDUFS1 to induce mitochondrial dysfunction and cardiomyocyte apoptosis. Our findings suggest that Akap1 upregulation has therapeutic potential for myocardial injury in individuals with diabetes.
Keyphrases
- oxidative stress
- type diabetes
- endoplasmic reticulum stress
- cell cycle arrest
- heart failure
- cell death
- wound healing
- cardiovascular disease
- cell proliferation
- poor prognosis
- replacement therapy
- glycemic control
- signaling pathway
- angiotensin ii
- metabolic syndrome
- high fat diet induced
- endothelial cells
- weight loss
- atrial fibrillation