108605
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.4 Breast Cancer (Dove Med Press)
- 3.2 Clin Epidemiol
- 2.6 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.7 Clin Interv Aging
- 5.1 Drug Des Dev Ther
- 3.1 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.6 Int J Women's Health
- 2.9 Neuropsych Dis Treat
- 2.8 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.2 Ther Clin Risk Manag
- 2.5 J Pain Res
- 3.0 Diabet Metab Synd Ob
- 3.2 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.0 Risk Manag Healthc Policy
- 4.1 J Inflamm Res
- 2.0 Int J Gen Med
- 3.4 J Hepatocell Carcinoma
- 3.0 J Asthma Allergy
- 2.2 Clin Cosmet Investig Dermatol
- 2.4 J Multidiscip Healthc
已发表论文
糖酵解代谢重编程在动脉粥样硬化中平滑肌细胞的作用及研究进展
Authors Sun Y, Zhang B, Liu F, Luan B, Ding Y
Received 27 June 2025
Accepted for publication 12 September 2025
Published 26 September 2025 Volume 2025:18 Pages 5803—5810
DOI https://doi.org/10.2147/IJGM.S550081
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Redoy Ranjan
Yurong Sun,1 Bin Zhang,2 Fengyi Liu,1 Bo Luan,2 Yanchun Ding1
1Department of Cardiovascular Medicine, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, 116021, People’s Republic of China; 2Department of Cardiovascular Medicine, Renmin Hospital of China Medical University, Shenyang, 110013, People’s Republic of China
Correspondence: Yanchun Ding, Department of Cardiovascular Medicine, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, 116021, People’s Republic of China, Email etc2280@163.com
Abstract: Atherosclerosis(AS) is a chronic vascular disease resulting from the combined effects of lipid deposition and inflammatory responses, in which the phenotypic plasticity of vascular smooth muscle cells (VSMCs) plays a central role in disease progression. Under aerobic conditions, VSMCs undergo a metabolic shift reminiscent of the “Warburg effect”, supporting their proliferation, migration, and phenotypic modulation through enhanced glycolytic flux. Despite its pathophysiological significance, the mechanistic interplay between glycolytic reprogramming in VSMCs and atherosclerotic progression remains inadequately systematized. This review aims to bridge this knowledge gap by synthesizing emerging evidence on how glycolysis orchestrates VSMCs remodeling and contributes to the clinical manifestations of AS. Furthermore, we explore the synergistic coupling between glycolytic metabolism and electrophysiological dynamics in VSMCs—an emerging area with transformative potential. Our methodology integrates multidimensional strategies: first, we delineate the metabolic drivers of VSMCs phenotypic switching in AS; second, we combine in vitro and in vivo models to elucidate the role of VSMCs glycolysis in diabetes-accelerated AS and in-stent restenosis; lastly, we investigate metaboloelectrophysiological crosstalk and ion channel regulation as central mechanisms. This synthesis provides a conceptual and mechanistic foundation for targeting glycolytic pathways in AS and its complications, offering novel avenues for therapeutic intervention.
Keywords: smooth muscle cells, glycolysis, atherosclerosis
1Department of Cardiovascular Medicine, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, 116021, People’s Republic of China; 2Department of Cardiovascular Medicine, Renmin Hospital of China Medical University, Shenyang, 110013, People’s Republic of China
Correspondence: Yanchun Ding, Department of Cardiovascular Medicine, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, 116021, People’s Republic of China, Email etc2280@163.com
Abstract: Atherosclerosis(AS) is a chronic vascular disease resulting from the combined effects of lipid deposition and inflammatory responses, in which the phenotypic plasticity of vascular smooth muscle cells (VSMCs) plays a central role in disease progression. Under aerobic conditions, VSMCs undergo a metabolic shift reminiscent of the “Warburg effect”, supporting their proliferation, migration, and phenotypic modulation through enhanced glycolytic flux. Despite its pathophysiological significance, the mechanistic interplay between glycolytic reprogramming in VSMCs and atherosclerotic progression remains inadequately systematized. This review aims to bridge this knowledge gap by synthesizing emerging evidence on how glycolysis orchestrates VSMCs remodeling and contributes to the clinical manifestations of AS. Furthermore, we explore the synergistic coupling between glycolytic metabolism and electrophysiological dynamics in VSMCs—an emerging area with transformative potential. Our methodology integrates multidimensional strategies: first, we delineate the metabolic drivers of VSMCs phenotypic switching in AS; second, we combine in vitro and in vivo models to elucidate the role of VSMCs glycolysis in diabetes-accelerated AS and in-stent restenosis; lastly, we investigate metaboloelectrophysiological crosstalk and ion channel regulation as central mechanisms. This synthesis provides a conceptual and mechanistic foundation for targeting glycolytic pathways in AS and its complications, offering novel avenues for therapeutic intervention.
Keywords: smooth muscle cells, glycolysis, atherosclerosis