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已发表论文
内皮代谢重编程将糖尿病与动脉粥样硬化联系起来
Received 11 September 2025
Accepted for publication 9 January 2026
Published 11 February 2026 Volume 2026:19 565805
DOI https://doi.org/10.2147/DMSO.S565805
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Rebecca Baqiyyah Conway
Yangze Pan, Jin Si
Department Endocrinology, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430077, People’s Republic of China
Correspondence: Jin Si, Department Endocrinology, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430077, People’s Republic of China, Email jinsi@hust.edu.cn
Abstract: Diabetic vascular complications are common and severe, worsening quality of life and long-term outcomes. In diabetes, chronic hyperglycemia together with dyslipidemia and hypertension reshapes endothelial metabolism and homeostasis. Endothelial cells shift the balance of glucose utilization, fatty acid oxidation, and mitochondrial function, and these metabolic changes bias endothelial behavior toward reduced nitric oxide bioavailability, oxidative stress, and a pro-inflammatory, pro-thrombotic state. Over time, maladaptive stress responses promote senescence, cell loss, and endothelial-to-mesenchymal transition, accelerating the initiation and progression of atherosclerotic plaques. This review summarizes how diabetic cues drive endothelial metabolic reprogramming and how this, in turn, links endothelial dysfunction to plaque formation, growth, and instability. We highlight key metabolic pathways and discuss how local hemodynamic forces at athero-prone regions further shape endothelial phenotypes and inflammatory signaling. Finally, we outline therapeutic opportunities that target endothelial metabolism and stress responses—including modulation of glycolytic flux, mitochondrial and redox-directed strategies, and pathway-level interventions that curb hypoxia and inflammatory programs. We emphasize translational priorities such as endothelium-selective delivery, biomarkers of endothelial metabolic state, and rigorous clinical testing to enable earlier and more effective prevention of diabetes-associated atherosclerotic disease.
Keywords: atherosclerosis, metabolic reprogramming, diabetes, endothelium
Department Endocrinology, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430077, People’s Republic of China
Correspondence: Jin Si, Department Endocrinology, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430077, People’s Republic of China, Email jinsi@hust.edu.cn
Abstract: Diabetic vascular complications are common and severe, worsening quality of life and long-term outcomes. In diabetes, chronic hyperglycemia together with dyslipidemia and hypertension reshapes endothelial metabolism and homeostasis. Endothelial cells shift the balance of glucose utilization, fatty acid oxidation, and mitochondrial function, and these metabolic changes bias endothelial behavior toward reduced nitric oxide bioavailability, oxidative stress, and a pro-inflammatory, pro-thrombotic state. Over time, maladaptive stress responses promote senescence, cell loss, and endothelial-to-mesenchymal transition, accelerating the initiation and progression of atherosclerotic plaques. This review summarizes how diabetic cues drive endothelial metabolic reprogramming and how this, in turn, links endothelial dysfunction to plaque formation, growth, and instability. We highlight key metabolic pathways and discuss how local hemodynamic forces at athero-prone regions further shape endothelial phenotypes and inflammatory signaling. Finally, we outline therapeutic opportunities that target endothelial metabolism and stress responses—including modulation of glycolytic flux, mitochondrial and redox-directed strategies, and pathway-level interventions that curb hypoxia and inflammatory programs. We emphasize translational priorities such as endothelium-selective delivery, biomarkers of endothelial metabolic state, and rigorous clinical testing to enable earlier and more effective prevention of diabetes-associated atherosclerotic disease.
Keywords: atherosclerosis, metabolic reprogramming, diabetes, endothelium