Cardiac β-adrenergic receptor regulation of mitochondrial function in heart failure.
- Author:
Ai-Ming LIU
1
;
Wen-Li XU
2
;
Han XIAO
1
;
Er-Dan DONG
1
Author Information
1. Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University; Institute of Advanced Clinical Medicine, Peking University; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
2. Research Center for Cardiopulmonary Rehabilitation, University of Health and Rehabilitation Sciences Qingdao Hospital (Qingdao Municipal Hospital); School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266071, China.
- Publication Type:English Abstract
- MeSH:
Heart Failure/physiopathology*;
Humans;
Receptors, Adrenergic, beta/physiology*;
Mitochondria, Heart/physiology*;
Animals;
Oxidative Stress/physiology*;
Myocytes, Cardiac/physiology*;
Apoptosis/physiology*;
Signal Transduction/physiology*
- From:
Acta Physiologica Sinica
2024;76(6):865-880
- CountryChina
- Language:Chinese
-
Abstract:
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.
