Shen Ruxin, Zhang Yingying
Qingdao Medical College, Qingdao University, Qingdao, Shandong 266000, P.R. China.
Department of Tuberculosis, Affiliated Nantong Hospital of Shanghai University, Nantong, Jiangsu 226000, P.R. China.
Int J Mol Med. 2025 Aug;56(2). doi: 10.3892/ijmm.2025.5561. Epub 2025 Jun 6.
This review delves into the intricate relationship between amino acid metabolism and inflammation in coronary heart disease (CHD). Research shows that disruptions in the metabolism of arginine, glutamate, branched‑chain amino acids (BCAAs) and tryptophan exacerbate CHD inflammation via immunometabolic reprogramming and oxidative stress. Nitric oxide (NO), produced from arginine metabolism, regulates CHD progression multifacetedly. Glutamate metabolism dysregulation harms cardiovascular health, while glutamine exerts cardioprotective effects after myocardial infarction. Elevated BCAA levels are associated with atherosclerosis development, and tryptophan and its metabolites have complex effects on CHD. Notably, amino acid metabolism intersects with the immune system, modulating the functions of T cells, B cells and macrophages. These immune cells are crucial for CHD‑related inflammation. Inflammatory markers like high‑sensitivity C‑reactive protein, interleukin family members, interferon‑γ and monocyte chemoattractant protein‑1 are closely linked to CHD pathogenesis and progression, facilitating risk assessment. Clinical research, including animal and human studies, and technological applications such as metabolomics, offer insights into CHD diagnosis, treatment and prevention. Dietary intervention and drug therapy targeting amino acid metabolism show potential. For example, L‑arginine supplementation has cardioprotective effects and novel NO donors like compound‑N6 hold promise. However, certain substances like triclocarban have adverse impacts, while colchicine is beneficial. In summary, while current research has advanced the understanding of CHD, significant knowledge gaps remain, particularly regarding rare amino acids and the connection between amino acid metabolism and non‑coding RNA. Future research could utilize metabolomics, genomics and artificial intelligence for personalized CHD management, representing a paradigm shift towards individualized precision medicine.
本综述深入探讨了冠心病（CHD）中氨基酸代谢与炎症之间的复杂关系。研究表明，精氨酸、谷氨酸、支链氨基酸（BCAAs）和色氨酸代谢的紊乱通过免疫代谢重编程和氧化应激加剧了冠心病炎症。精氨酸代谢产生的一氧化氮（NO）多方面调节冠心病的进展。谷氨酸代谢失调损害心血管健康，而谷氨酰胺在心肌梗死后发挥心脏保护作用。BCAAs水平升高与动脉粥样硬化发展相关，色氨酸及其代谢产物对冠心病有复杂影响。值得注意的是，氨基酸代谢与免疫系统相互作用，调节T细胞、B细胞和巨噬细胞的功能。这些免疫细胞对冠心病相关炎症至关重要。高敏C反应蛋白、白细胞介素家族成员、干扰素-γ和单核细胞趋化蛋白-1等炎症标志物与冠心病发病机制和进展密切相关，有助于风险评估。包括动物和人体研究在内的临床研究以及代谢组学等技术应用为冠心病的诊断、治疗和预防提供了见解。针对氨基酸代谢的饮食干预和药物治疗显示出潜力。例如，补充L-精氨酸具有心脏保护作用，新型NO供体如化合物-N6前景广阔。然而，某些物质如三氯生有不利影响，而秋水仙碱有益。总之，虽然目前的研究增进了对冠心病的理解，但仍存在重大知识空白，特别是关于稀有氨基酸以及氨基酸代谢与非编码RNA之间的联系。未来的研究可以利用代谢组学、基因组学和人工智能进行冠心病个性化管理，这代表着向个体化精准医学的范式转变。
