Syntaxin 17 Translocation Mediated Mitophagy Switching Drives Hyperglycemia-Induced Vascular Injury
文献类型： 外文期刊
作者： Luo, Anqi 1 ; Wang, Rui 2 ; Gong, Jingwen 3 ; Wang, Shuting 3 ; Yun, Chuan 4 ; Chen, Zongcun 5 ; Jiang, Yanan 6 ; Liu, Xiaoquan 1 ; Dai, Haofu 7 ; Liu, Haochen 1 ; Zheng, Yunsi 2 ;
作者机构： 1.China Pharmaceut Univ, Sch Pharm, Nanjing 211198, Peoples R China
2.Hainan Med Univ, Key Lab Hainan Trauma & Disaster Rescue, Haikou 571199, Peoples R China
3.Hainan Med Univ, Sch Pharm, Haikou 571199, Peoples R China
4.Hainan Med Univ, Affiliated Hosp 1, Clin Res Ctr Metab Dis, Haikou 570102, Peoples R China
5.Hainan Med Univ, Affiliated Hosp 2, Dept Endocrinol, Haikou 570311, Peoples R China
6.Hainan Med Univ, Affiliated Hosp 2, Dept Pharm, Haikou 570311, Peoples R China
7.Chinese Acad Trop Agr Sci, Hainan Key Lab Res & Dev Nat Prod Li Folk Med, Haikou 571101, Peoples R China
关键词： (diabetes; Fis1; mitophagy; Syntaxin 17); vascular endothelial injury
期刊名称：ADVANCED SCIENCE （ 影响因子：14.1； 五年影响因子：15.6 ）
ISSN：
年卷期： 2025 年 12 卷 19 期
页码：
收录情况： SCI
摘要： The risk of diabetic cardiovascular complications is closely linked to the length of hyperglycemia exposure. Mitophagy plays a significant role in vascular endothelial injury. However, the specific mechanisms by which mitophagy contributes to endothelial injury during sustained hyperglycemia remain unclear. In diabetic ApoE(-/- )mice and human umbilical vein endothelial cell (HUVEC) models, mitophagy is enhanced following short-term and long-term high-glucose exposure. Short-term high-glucose exposure promotes Parkin-mediated mitophagy and upregulates mitochondrial fission protein 1 (Fis1) expression, whereas long-term high-glucose exposure suppresses Parkin-mediated mitophagy and downregulates Fis1. With prolonged high-glucose exposure, Syntaxin 17 (STX17) translocates from the endoplasmic reticulum to the mitochondria, activating STX17-mediated mitophagy. Silencing STX17 alleviates mitochondrial degradation, decreases reactive oxygen species (ROS) levels, enhances endothelial nitric oxide synthase (eNOS) phosphorylation, and reduces apoptosis. Silencing Fis1 accelerates the switching to STX17-mediated mitophagy, worsening endothelial dysfunction, whereas Fis1 overexpression prevents this switching, reducing ROS and apoptosis and enhancing eNOS phosphorylation. In summary, these findings suggest that the switching from Parkin-mediated to STX17-mediated mitophagy drives vascular endothelial injury following long-term hyperglycemic exposure, providing valuable insights into therapeutic strategies for diabetic cardiovascular complications.
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