Cardiac β-adrenergic receptor regulation of mitochondrial function in heart failure
Heart failure is characterized by abnormal β-adrenergic receptor(β-AR)activation and mitochondrial dysfunction.In heart failure,overactivation of β-AR mediates key pathological processes in cardiomyocytes,including oxidative stress,calcium overload and metabolic abnormalities,which subsequently lead to inflammation,myocardial apoptosis and necrosis.Mitochondria are the core organelles for energy metabolism,and also play a vital role in calcium homeostasis,redox balance and signaling transduction.Moderate β-AR activation is conducive to maintaining mitochondrial homeostasis and physiological cardiomyocyte function.However,β-AR overactivation in heart failure disrupts mitochondrial function through multiple mechanisms.Therefore,our review aims to elucidate how β-AR regulates mitochondrial function,particularly under sympathetic stress,impacting oxidative stress,apoptosis,necrosis,and metabolic imbalance.By describing these mechanisms,we seek to propose new insights and therapeutic targets for the prevention and treatment of heart failure.
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