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Published on: December 7, 2017
Glucose Metabolism Reprogramming of Vascular Endothelial Cells and Its Implication in Development of Atherosclerosis
Shiwen Luo1, Liu Li1, Huiqing Chen1
1Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, 410208 Changsha, Hunan, China.
Insights
Glucose metabolism reprogramming in vascular endothelial cells (VECs) drives atherosclerosis (AS) development by impairing VEC function. Understanding this process offers new therapeutic targets for cardiovascular diseases.
Area of Science:
- Cardiovascular Biology
- Metabolic Disease Research
- Endothelial Cell Biology
Background:
- Atherosclerosis (AS) is a major cause of cardiovascular morbidity and mortality.
- Damage to vascular endothelial cells (VECs), the blood vessel lining, initiates AS.
- VECs rely on aerobic glycolysis, but diseases alter this metabolism.
Purpose of the Study:
- To review how VEC glucose metabolism reprogramming promotes AS.
- To explore the molecular mechanisms linking altered VEC metabolism to AS pathogenesis.
- To identify potential therapeutic targets for AS prevention and treatment.
Main Methods:
- Literature review of studies on VEC glucose metabolism and AS.
- Analysis of molecular pathways involved in VEC metabolic reprogramming.
- Synthesis of evidence linking VEC dysfunction to AS progression.
Main Results:
- Altered VEC glucose metabolism reprogramming is central to AS development.
- This reprogramming induces VEC barrier dysfunction, affecting endothelial integrity.
- It also influences VEC autophagy, inflammatory responses, and proliferation, contributing to AS.
Conclusions:
- VEC glucose metabolism reprogramming is a key driver of atherosclerosis.
- Targeting VEC metabolic pathways may offer novel strategies for AS treatment.
- Further research into these mechanisms could yield new therapeutic interventions.
Abstract:
Atherosclerosis (AS) is an important cause of morbidity and mortality in cardiovascular diseases such as coronary atherosclerotic heart disease and stroke. As the primary natural barrier between blood and the vessel wall, damage to vascular endothelial cells (VECs) is one of the initiating factors for the development of AS. VECs primarily use aerobic glycolysis for energy supply, but several diseases can cause altered glucose metabolism in VECs. Glucose metabolism reprogramming of VECs is the core event of AS, which is closely related to the development of AS. In this review, we review how glucose metabolism reprogramming of VECs promotes the development of AS by inducing VEC barrier dysfunction, autophagy, altering the inflammatory response, and proliferation of VECs, in the hopes of providing new ideas and discovering new targets for the prevention and treatment of AS.
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