{"title":"氨基酸代谢与冠心病炎症的关系(综述)。","authors":"Ruxin Shen, Yingying Zhang","doi":"10.3892/ijmm.2025.5561","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176267/pdf/","citationCount":"0","resultStr":"{\"title\":\"Relationship between amino acid metabolism and inflammation in coronary heart disease (Review).\",\"authors\":\"Ruxin Shen, Yingying Zhang\",\"doi\":\"10.3892/ijmm.2025.5561\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":14086,\"journal\":{\"name\":\"International journal of molecular medicine\",\"volume\":\"56 2\",\"pages\":\"\"},\"PeriodicalIF\":5.7000,\"publicationDate\":\"2025-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176267/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International journal of molecular medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/ijmm.2025.5561\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/6/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of molecular medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/ijmm.2025.5561","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/6 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Relationship between amino acid metabolism and inflammation in coronary heart disease (Review).
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.
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