Heart-type fatty acid mediated lipid signaling and metabolic remodeling in coronary heart disease.

Coronary heart disease (CHD) is closely associated with lipid metabolic disorders, inflammatory activation, and myocardial energy imbalance. Heart-type fatty acid-binding protein (H-FABP), a major intracellular fatty acid transporter in cardiomyocytes, plays a critical role in fatty acid trafficking, mitochondrial β-oxidation, and lipid signaling. Under pathological conditions such as hypoxia, oxidative stress, and inflammation, H-FABP dysfunction disrupts lipid homeostasis, leading to lipotoxicity, mitochondrial impairment, endothelial injury, and microcirculatory dysfunction. These pathological features are highly consistent with intermingled phlegm blood stasis (IPBS) syndrome in CHD. This review summarizes the structural characteristics, transport mechanisms, and signaling functions of H-FABP, with emphasis on its roles in metabolic remodeling, inflammatory responses, and ischemic injury. Emerging evidence indicates that circulating H-FABP levels are strongly associated with dyslipidemia, coronary lesion severity, and adverse cardiovascular outcomes. Mechanistically, impaired H-FABP-mediated fatty acid transport may serve as a molecular link between lipid metabolic dysregulation and IPBS progression. Therefore, H-FABP is proposed as both a mechanistic biomarker and a potential therapeutic target in CHD. Further investigation of H-FABP-related signaling pathways may provide new insights into metabolism-driven cardiovascular injury and support the development of precision diagnostic and therapeutic strategies.