- Author:
Qiong WANG
1
;
Jia-Yang ZHANG
2
;
Le-Jia QIU
1
;
Li-Hong CHEN
1
Author Information
- Publication Type:English Abstract
- MeSH: Humans; Heart Failure/physiopathology*; Circadian Rhythm/physiology*; Circadian Clocks/physiology*; ARNTL Transcription Factors/physiology*; Nuclear Receptor Subfamily 1, Group D, Member 1/physiology*; Oxidative Stress; Energy Metabolism; Animals
- From: Acta Physiologica Sinica 2025;77(4):653-668
- CountryChina
- Language:Chinese
- Abstract: The circadian clock is an endogenous time-keeping system that maintains physiological homeostasis by integrating environmental and genetic interactions. Heart failure is a complex clinical syndrome characterized by structural abnormalities and/or functional impairment of the heart. Growing evidence suggests that core circadian components, such as BMAL1 and REV-ERBα, play important roles in modulating myocardial energy metabolism, inflammatory responses, and oxidative stress, contributing to myocardial structural and metabolic remodeling during heart failure progression. Notably, circadian disruption is closely associated with heart failure, with aberrant blood pressure rhythms and disturbances in the sleep-wake cycle in patients. The time-dependent efficacy of heart failure medications further supports the potential of chronotherapy-based strategies to improve clinical outcomes. Here, we summarize the multifaceted regulatory roles of the circadian clock, particularly core clock genes, in heart failure pathogenesis, providing a theoretical framework for developing personalized chronotherapeutic strategies for heart failure management.

