Succinate predisposes mice to atrial fibrillation by impairing mitochondrial function via SUCNR1/AMPK axis.

ABSTRACT: Atrial fibrillation (AF), a major public health concern, is associated with high rates of death and disability. Mitochondrial dysfunction has emerged as a key contributor to the pathophysiology of AF. Succinate, an essential Krebs cycle metabolite, is often elevated in the circulation of patients at risk for AF. However, its exact role in AF pathogenesis is still not well understood. To explore the association linking succinate overload and AF, we first established AF-susceptible mouse models of obesity and diabetes, confirming that circulating succinate levels were significantly elevated in these AF-prone mice. Next, we assessed AF vulnerability and atrial remodeling in succinate-treated mice (2 %/5 % for 7 weeks) or isolated primary atrial cells (0.5 mM for 24 h). Our results demonstrate

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC11915173 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature