TMEM65 ameliorates post-myocardial infarction heart failure by maintaining mitochondrial calcium homeostasis via inhibiting NCLX ubiquitination
Disruption of mitochondrial calcium homeostasis drives post-myocardial infarction (MI) heart failure by impairing excitation-contraction coupling . However, the critical upstream molecular mechanisms remain unclear, necessitating novel interventional targets. To elucidate the core mechanisms driving cardio...