Chen Li, Chen Mingtai, Yang Xinrui, Hu Yuanli, Qiu Caiwei, Fu Youyou, Lan Xiaoyu, Luo Gang, Liu Qiuyu, Liu Mengnan
The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, Sichuan, China.
Department of Cardiovascular Disease, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, Guangdong, China.
Front Endocrinol (Lausanne). 2025 Jun 5;16:1617305. doi: 10.3389/fendo.2025.1617305. eCollection 2025.
Cardiovascular diseases (CVDs) remain the leading cause of global mortality, yet their pathogenesis has not been fully elucidated, particularly regarding the role of abnormal energy metabolism. Major outstanding questions pertain to the dynamic regulation of metabolic reprogramming and its complex interplay with mitochondrial dysfunction. Previous studies have demonstrated that the heart, as a high-energy-demand organ, relies on the dynamic equilibrium of substrates such as fatty acid (FA) and glucose to sustain adenosine triphosphate (ATP) production. Metabolic disturbances-characterized by suppressed FA oxidation and aberrant activation of glycolysis-directly contribute to the pathological progression of various CVDs, including heart failure (HF), atherosclerosis, and myocardial infarction(MI), through mechanisms involving oxidative stress, inflammatory responses, and an energy crisis. This review systematically examines the core pathways of cardiac energy metabolism (e.g., mitochondrial oxidative phosphorylation (OXPHOS), regulation of glucose and lipid metabolism) and their dysregulation in disease states, while evaluating intervention strategies targeting metabolic pathways, such as mitochondrial function enhancement and substrate utilization modulation. Future research directions emphasize the integration of metabolomics with clinical translational studies to comprehensively decipher the multidimensional regulation of metabolic networks, thereby facilitating the development of novel precision therapeutic targets.
心血管疾病（CVDs）仍然是全球死亡的主要原因，但其发病机制尚未完全阐明，特别是关于异常能量代谢的作用。主要悬而未决的问题涉及代谢重编程的动态调节及其与线粒体功能障碍的复杂相互作用。先前的研究表明，心脏作为一个高能量需求器官，依赖脂肪酸（FA）和葡萄糖等底物的动态平衡来维持三磷酸腺苷（ATP）的产生。以脂肪酸氧化受抑制和糖酵解异常激活为特征的代谢紊乱，通过涉及氧化应激、炎症反应和能量危机的机制，直接促成各种心血管疾病（包括心力衰竭（HF）、动脉粥样硬化和心肌梗死（MI））的病理进展。本综述系统地研究了心脏能量代谢的核心途径（如线粒体氧化磷酸化（OXPHOS）、葡萄糖和脂质代谢的调节）及其在疾病状态下的失调，同时评估针对代谢途径的干预策略，如增强线粒体功能和调节底物利用。未来的研究方向强调代谢组学与临床转化研究的整合，以全面解读代谢网络的多维调节，从而促进新型精准治疗靶点的开发。
