Glycolysis and neutrophil extracellular traps in atherosclerosis: Mechanisms, association, and therapeutic strategies.
L, L., X, Z., Z, Y., X, L., C, S., L, H., K, Z., X, L., Y, Y., & M, W. (2026). Glycolysis and neutrophil extracellular traps in atherosclerosis: Mechanisms, association, and therapeutic strategies.. International journal of immunopathology and pharmacology. https://doi.org/10.1177/03946320261450099
L L, X Z, Z Y, X L, C S, L H, et al. Glycolysis and neutrophil extracellular traps in atherosclerosis: Mechanisms, association, and therapeutic strategies.. International journal of immunopathology and pharmacology. 2026; doi: 10.1177/03946320261450099
L L, X Z, Z Y, et al. Glycolysis and neutrophil extracellular traps in atherosclerosis: Mechanisms, association, and therapeutic strategies.[J]. International journal of immunopathology and pharmacology. 2026. DOI: 10.1177/03946320261450099.
@article{l2026,
author = {Li L and Zhang X and Yu Z and Li X and Sun C and Hu L and Zhou K and Liu X and Yuan Y and Wu M},
title = {Glycolysis and neutrophil extracellular traps in atherosclerosis: Mechanisms, association, and therapeutic strategies.},
journal = {International journal of immunopathology and pharmacology},
year = {2026},
doi = {10.1177/03946320261450099},
note = {PMID: 42199005},
}
TY - JOUR AU - Li L AU - Zhang X AU - Yu Z AU - Li X AU - Sun C AU - Hu L AU - Zhou K AU - Liu X AU - Yuan Y AU - Wu M TI - Glycolysis and neutrophil extracellular traps in atherosclerosis: Mechanisms, association, and therapeutic strategies. T2 - International journal of immunopathology and pharmacology PY - 2026 DO - 10.1177/03946320261450099 AN - PMID:42199005 ER -
Atherosclerosis (AS) is a chronic inflammatory disorder of the medium and large arteries, characterized by lipid accumulation within the arterial wall and a sustained inflammatory milieu, and it remains a leading cause of cardiovascular morbidity and mortality worldwide. Glycolysis and neutrophil extracellular traps (NETs) are both involved in the initiation and progression of AS in part through effects on endothelial function, platelet activation, lipid metabolism, and the inflammatory microenvironment. This article reviews the roles of NETs and glycolysis in AS, elucidates the mechanisms underlying NETosis, and discusses the association between glycolysis and NETosis. Finally, the article discusses the potential value of glycolytic inhibitors in the treatment of AS, with the aim of providing new perspectives for the diagnosis and treatment of AS and related cardiovascular diseases.