Suppr超能文献

嘌呤能受体介导内皮功能障碍,并参与动脉粥样硬化。

Purinergic receptors mediate endothelial dysfunction and participate in atherosclerosis.

机构信息

Hunan University of Chinese Medicine, Changsha, 410208, China.

Guizhou University of Traditional Chinese Medicine, Guiyang, 550025, China.

出版信息

Purinergic Signal. 2023 Mar;19(1):265-272. doi: 10.1007/s11302-021-09839-x. Epub 2022 Jan 3.

Abstract

Atherosclerosis is the main pathological basis of cardiovascular disease and involves damage to vascular endothelial cells (ECs) that results in endothelial dysfunction (ED). The vascular endothelium is the key to maintaining blood vessel health and homeostasis. ED is a complex pathological process involving inflammation, shear stress, vascular tone, adhesion of leukocytes to ECs, and platelet aggregation. The activation of P2X4, P2X7, and P2Y2 receptors regulates vascular tone in response to shear stress, while activation of the A2A, P2X4, P2X7, P2Y1, P2Y2, P2Y6, and P2Y12 receptors promotes the secretion of inflammatory cytokines. Finally, P2X1, P2Y1, and P2Y12 receptor activation regulates platelet activity. These purinergic receptors mediate ED and participate in atherosclerosis. In short, P2X4, P2X7, P2Y1, and P2Y12 receptors are potential therapeutic targets for atherosclerosis.

摘要

动脉粥样硬化是心血管疾病的主要病理学基础,涉及血管内皮细胞(EC)的损伤,导致内皮功能障碍(ED)。血管内皮是维持血管健康和内稳态的关键。ED 是一个涉及炎症、切应力、血管张力、白细胞与 EC 黏附以及血小板聚集的复杂病理过程。P2X4、P2X7 和 P2Y2 受体的激活调节了对切应力的血管张力,而 A2A、P2X4、P2X7、P2Y1、P2Y2、P2Y6 和 P2Y12 受体的激活促进了炎症细胞因子的分泌。最后,P2X1、P2Y1 和 P2Y12 受体的激活调节血小板活性。这些嘌呤能受体介导 ED 并参与动脉粥样硬化。总之,P2X4、P2X7、P2Y1 和 P2Y12 受体是动脉粥样硬化的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/01d6/9984579/aaf68ac487f9/11302_2021_9839_Fig1_HTML.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验