瞬时受体电位1型香草素:糖尿病模型中的心脏保护作用。

Channels (Austin, Tex.) Pub Date : 2023-12-01 Epub Date: 2023-11-20 DOI:10.1080/19336950.2023.2281743
Jiaqi Bao, Zhicheng Gao, Yilan Hu, Lifang Ye, Lihong Wang
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引用次数: 0

摘要

心血管疾病,尤其是心力衰竭(HF)是糖尿病患者死亡的主要原因。糖尿病患者容易患一种特殊类型的心肌病,称为糖尿病性心肌病(DCM),这种病不能用高血压或冠状动脉疾病等心脏病来解释,并可能导致心力衰竭。不幸的是,目前糖尿病相关心血管并发症的治疗策略主要是控制血糖水平;然而,心脏结构和功能的改善并不理想。瞬时受体电位阳离子通道亚家族V成员1 (TRPV1)是一种非选择性阳离子通道,已被证明在心血管系统中普遍表达。越来越多的证据表明,TRPV1通道的激活对心血管系统具有潜在的保护作用。大量研究表明,激活TRPV1通道可以改善糖尿病相关并发症的发生和进展,包括心肌病;然而,具体的机制和影响尚不清楚。本文综述了TRPV1通道激活在糖尿病模型心脏中从氧化/硝化应激、线粒体功能、内皮功能、炎症和心脏能量代谢等方面发挥保护作用,抑制DCM的发生和进展。因此,TRPV1可能成为预防和治疗糖尿病引起的心血管并发症的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transient receptor potential vanilloid type 1: cardioprotective effects in diabetic models.

Cardiovascular disease, especially heart failure (HF) is the leading cause of death in patients with diabetes. Individuals with diabetes are prone to a special type of cardiomyopathy called diabetic cardiomyopathy (DCM), which cannot be explained by heart diseases such as hypertension or coronary artery disease, and can contribute to HF. Unfortunately, the current treatment strategy for diabetes-related cardiovascular complications is mainly to control blood glucose levels; nonetheless, the improvement of cardiac structure and function is not ideal. The transient receptor potential cation channel subfamily V member 1 (TRPV1), a nonselective cation channel, has been shown to be universally expressed in the cardiovascular system. Increasing evidence has shown that the activation of TRPV1 channel has a potential protective influence on the cardiovascular system. Numerous studies show that activating TRPV1 channels can improve the occurrence and progression of diabetes-related complications, including cardiomyopathy; however, the specific mechanisms and effects are unclear. In this review, we summarize that TRPV1 channel activation plays a protective role in the heart of diabetic models from oxidation/nitrification stress, mitochondrial function, endothelial function, inflammation, and cardiac energy metabolism to inhibit the occurrence and progression of DCM. Therefore, TRPV1 may become a latent target for the prevention and treatment of diabetes-induced cardiovascular complications.

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