Distinct Effects of Mitochondrial Na⁺/Ca²⁺ Exchanger Inhibition and Ca²⁺ Uniporter Activation on Ca²⁺ Sparks and Arrhythmogenesis in Diabetic Rats.

ABSTRACT: Background Mitochondrial dysfunction contributes to the cardiac remodeling triggered by type 2 diabetes (T2D). Mitochondrial Ca²⁺ concentration ([Ca²⁺]_m) modulates the oxidative state and cytosolic Ca²⁺ regulation. Thus, we investigated how T2D affects mitochondrial Ca²⁺ fluxes, the downstream consequences on myocyte function, and the effects of normalizing mitochondrial Ca²⁺ transport. Methods and Results We compared myocytes/hearts from transgenic rats with late-onset T2D (rats that develop late-onset T2D due to heterozygous expression of human amylin in the pancreatic β-cells [HIP] model) and their nondiabetic wild-type (WT) littermates. [Ca²⁺]_m was significantly lower in myocytes from diabetic HIP r

SUBMITTER: Velmurugan S 

PROVIDER: S-EPMC10382117 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature