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作者

Ke Li, Shaohu Wang, Jiana Li, Lingling Wang, Qin Zhang, Liming Hou, Xinyi Yu, Zhendong Liu, Ting Lv, Luxiang Shang

作者单位

Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan 250014, China com. ⁷ School of Clinical and Basic Medical Sciences, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan 250117, China Affiliations ¹ Department of Gastroenterology, 215 Hospital of Shaanxi Province, Xianyang 712000, China Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250117, China. Electronic address: shangluxiang@16 Department of Gastroenterology, No.983rd Hospital of the Chinese People's Liberation Army Joint Logistics and Security Forces, Tianjin 300143, China. ⁴ Department of Gastroenterology, 215 Hospital of Shaanxi Province, Xianyang 712000, China. ⁵ School of Clinical and Basic Medical Sciences, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan 250117, China. ⁶ Department of Gastroenterology, 215 Hospital of Shaanxi Province, Xianyang 712000, China. Electronic address: xy215lt@16 School of Clinical and Basic Medical Sciences, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan 250117, China. ² School of Clinical and Basic Medical Sciences, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan 250117, China Department of Immunization and Planning, Heping District Center for Disease Control and Prevention, Tianjin 300041, China. ³ School of Clinical and Basic Medical Sciences, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan 250117, China com.

刊名

Experimental cell research

年份

2025

页码

114410

ISSN

1090-2422

关键词

Apoptosis HSP70 MicroRNA Oxidative stress Shear stress.

摘要

Atherosclerosis is a chronic disease initiated by vascular endothelial dysfunction, with low shear stress being a critical inducing factor in this dysfunction. Apoptosis, a form of programmed cell death, is closely associated with AS progression. However, the impact of low SS on endothelial apoptosis and its specific molecular mechanisms remains unclear. Our study revealed that low SS induces apoptosis in endothelial cells and contributes to endothelial dysfunction. Under low SS conditions, mi...更多

Atherosclerosis is a chronic disease initiated by vascular endothelial dysfunction, with low shear stress being a critical inducing factor in this dysfunction. Apoptosis, a form of programmed cell death, is closely associated with AS progression. However, the impact of low SS on endothelial apoptosis and its specific molecular mechanisms remains unclear. Our study revealed that low SS induces apoptosis in endothelial cells and contributes to endothelial dysfunction. Under low SS conditions, miR-330 expression was markedly upregulated, which subsequently targeted and inhibited SOD2 expression, leading to ROS accumulation and oxidative stress. Overexpression of SOD2 under low SS conditions markedly elevated HSP70 expression, contributing to endothelial homeostasis. However, when HSP70 expression was inhibited in the context of SOD2 overexpression, there was a significant increase in pro-apoptotic proteins and total apoptosis rate, along with a significant reduction in endothelial function markers such as nitric oxide and endothelial nitric oxide synthase. Notably, our experiments indicated no direct interaction between SOD2 and HSP70. Furthermore, inhibiting ROS production significantly raised HSP70 expression, suggesting that SOD2 regulates HSP70 in an indirect process involving ROS. In summary, our findings elucidate that low SS induces endothelial apoptosis and dysfunction through the miR-330/SOD2/HSP70 signaling pathway, providing valuable insights into AS intervention and prevention.收起

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