Authors
Haoshuang Li, Anni Song, Jiachen Zhang, Hongwei Dong, Xiaoci Li, Ying Zhao
Published in
Cardiovascular drugs and therapy. Sep 10, 2026. Epub Sep 10, 2026.
Abstract
The progression of atherosclerosis is closely associated with alterations in cellular glucose metabolism and vascular immunometabolic regulation. Increasing evidence indicates that glycometabolic reprogramming in macrophages, ECs, and vascular smooth muscle cells contributes to plaque development by modulating inflammatory activation, oxidative stress, lipid metabolism, and cellular phenotypic changes. In this review, we summarize recent advances in glycometabolic reprogramming during atherosclerosis, focusing on glycolysis, the pentose phosphate pathway, and lactate-mediated epigenetic regulation. We further discuss how metabolic alterations interact with immune responses, trained immunity, epigenetic remodeling, and cellular senescence to regulate the atherosclerotic microenvironment. In addition, we highlight potential therapeutic targets involved in metabolic regulation, including key glycolytic enzymes such as 6-phosphofructo-2-kinase and lactate dehydrogenase A, as well as metabolic-epigenetic pathways such as the TRAP1/HDAC3/H4K12la axis. However, significant challenges remain regarding cell-type specificity, therapeutic selectivity, and clinical translation of metabolic interventions. Understanding the complex relationship between glycometabolic reprogramming and vascular immunometabolism can provide mechanistic insights and guide future investigations of metabolic interventions for atherosclerosis.
PMID:
42720722
Bibliographic data and abstract were imported from PubMed on 10 Sep 2026.
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