Department of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Department of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA; Center of Excellence for Inflammation, Infectious Disease and Immunity, East Tennessee State University, Johnson City, TN 37614, USA; James H Quillen Veterans Affairs Medical Center, Mountain Home, TN 37684, USA.
Curr Opin Pharmacol. 2020 Oct;54:27-35. doi: 10.1016/j.coph.2020.06.007. Epub 2020 Aug 1.
Heart failure is a leading cause of death in the United States. Diabetes, also known as diabetes mellitus (DM), exponentially increases the risk of heart failure. The increase in oxidative stress and metabolic dysfunction caused by DM can lead to DNA damage and the development of diabetic cardiomyopathy. Ataxia telangiectasia mutated kinase (ATM) is a DNA damage response protein with a primary nuclear function to regulate cell cycle progression in response to double-strand DNA breaks, acts as a redox sensor, and facilitates DNA repair. ATM deficiency associates with the development of insulin resistance and DM. Consequently, patients with Ataxia telangiectasia, a rare autosomal recessive disorder, have an increased risk of developing heart failure. The main objective of this review is to summarize the shared metabolic and cardiac abnormalities associated with DM and ATM deficiency, with a focus on the development of heart failure.
心力衰竭是美国的主要死亡原因之一。糖尿病,又称糖尿病(DM),会使心力衰竭的风险呈指数级增加。DM 引起的氧化应激和代谢功能障碍会导致 DNA 损伤和糖尿病心肌病的发展。共济失调毛细血管扩张突变激酶(ATM)是一种 DNA 损伤反应蛋白,主要核功能是调节细胞周期进程以响应双链 DNA 断裂,作为氧化还原传感器,并促进 DNA 修复。ATM 缺乏与胰岛素抵抗和 DM 的发展有关。因此,患有罕见的常染色体隐性遗传病共济失调毛细血管扩张症的患者发生心力衰竭的风险增加。本综述的主要目的是总结与 DM 和 ATM 缺乏相关的共同代谢和心脏异常,重点是心力衰竭的发展。