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The rising global incidence of cardiovascular diseases (CVDs) poses a serious challenge to public health systems, and there is an urgent need to alleviate this disease burden through innovative treatment strategies. Cardiomyocyte energy metabolism is highly dependent on fatty acid β-oxidation (FAO), which is a process that releases energy in the form of ATP. Impaired FAO not only reduces ATP generation but also induces pathological lipid deposition in cardiomyocytes, leading to cardiac dysfunction. As a selective autophagic process responsible for intracellular lipid droplet degradation, lipophagy serves as a critical regulator of myocardial energetic homeostasis through its coordination of the dynamic balance between lipolytic metabolism and fatty acid oxidation. Although lipophagy serves as a key regulatory node for fatty acid metabolism and maintains core functions in cardiovascular homeostasis, its precise pathological mechanisms in cardiovascular diseases remain incompletely clarified. The bidirectional regulatory mode of lipophagy, together with the causal regulation between fatty acid metabolic flux and lipotoxicity accumulation, is critical for dissecting molecular pathogenesis of cardiovascular lesions. This review systematically integrates and analyzes the bidirectional regulatory networks of various lipophagy subtypes, and summarizes cutting-edge research progress in cardiovascular diseases such as atherosclerosis, myocardial ischemia-reperfusion injury and diabetic cardiomyopathy. It provides theoretical basis for developing novel cardiovascular disease treatment strategies targeting lipophagy pathways.
Wu et al. (Tue,) studied this question.