激活素受体样激酶7通过激活糖尿病动脉粥样硬化中的Smad2/3信号通路促进血管平滑肌细胞凋亡。
Activin receptor-like kinase 7 promotes apoptosis of vascular smooth muscle cells activating Smad2/3 signaling in diabetic atherosclerosis.
作者信息
Cao Shengchuan, Yuan Qiuhuan, Dong Qianqian, Liu Xilong, Liu Weikang, Zhai Xiaoxuan, Zhang Chuanxin, Liu Han, Tang Mengxiong, Wei Shujian, Chen Yuguo
机构信息
Department of Emergency Medicine, Qilu Hospital of Shandong University, Jinan, China.
Shandong Provincial Clinical Research Center for Emergency and Critical Care Medicine, Institute of Emergency and Critical Care Medicine of Shandong University, Chest Pain Center, Qilu Hospital of Shandong University, Jinan, China.
出版信息
Front Pharmacol. 2022 Aug 17;13:926433. doi: 10.3389/fphar.2022.926433. eCollection 2022.
Vascular smooth muscle cells (VSMCs) is a vital accelerator in the late phase of diabetic atherosclerosis, but the underlying mechanism remains unclear. The aim of our study was to investigate whether activin receptor-like kinase 7 (ALK7)-Smad2/3 pathway plays an important role in VSMC apoptosis of diabetic atherosclerosis. It was shown that ALK7 expression was obviously elevated in the aorta of ApoE mice with type 2 diabetes mellitus. Inhibition of ALK7 expression significantly improved the stability of atherosclerotic plaques and reduced cell apoptosis. Further experiments showed that ALK7 knockdown stabilized atherosclerotic plaques by reducing VSMC apoptosis via activating Smad2/3. Our study uncovered the important role of ALK7-Smad2/3 signaling in VSMCs apoptosis, which might be a potential therapeutic target in diabetic atherosclerosis.
血管平滑肌细胞（VSMCs）是糖尿病动脉粥样硬化晚期的重要促进因素，但其潜在机制仍不清楚。我们研究的目的是探讨激活素受体样激酶7（ALK7）-Smad2/3信号通路在糖尿病动脉粥样硬化的血管平滑肌细胞凋亡中是否起重要作用。结果显示，在2型糖尿病ApoE小鼠的主动脉中，ALK7表达明显升高。抑制ALK7表达可显著改善动脉粥样硬化斑块的稳定性并减少细胞凋亡。进一步实验表明，ALK7基因敲低通过激活Smad2/3减少血管平滑肌细胞凋亡，从而稳定动脉粥样硬化斑块。我们的研究揭示了ALK7-Smad2/3信号在血管平滑肌细胞凋亡中的重要作用，这可能是糖尿病动脉粥样硬化的一个潜在治疗靶点。
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