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高血压与血脂异常:内皮相关犯罪的两大帮凶。

Hypertension and Dyslipidemia: the Two Partners in Endothelium-Related Crime.

机构信息

Center of Translational Medicine, Medical University of Gdańsk, Dębinki 7, 80-952, Gdańsk, Poland.

Department of Hypertension and Diabetology, Medical University of Gdańsk, Smoluchowskiego 17, 80-214, Gdańsk, Poland.

出版信息

Curr Atheroscler Rep. 2023 Sep;25(9):605-612. doi: 10.1007/s11883-023-01132-z. Epub 2023 Aug 18.

Abstract

PURPOSE OF REVIEW

The goal of this article is to characterize the endothelium's role in the development of hypertension and dyslipidemia and to point out promising therapeutic directions.

RECENT FINDINGS

Dyslipidemia may facilitate the development of hypertension, whereas the collaboration of these two silent killers potentiates the risk of atherosclerosis. The common pathophysiological denominator for hypertension and dyslipidemia is endothelial cell dysfunction, which manifests as dysregulation of homeostasis, redox balance, vascular tone, inflammation, and thrombosis. Treatment focused on mediators acting in these processes might be groundbreaking. Metabolomic research on hypertension and dyslipidemia has revealed new therapeutic targets. State-of-the-art solutions integrating interview, clinical examination, innovative imaging, and omics profiles along with artificial intelligence have been already shown to improve patients' risk stratification and treatment. Pathomechanisms underlying hypertension and dyslipidemia take place in the endothelium. Novel approaches involving endothelial biomarkers and bioinformatics advances could open new perspectives in patient management.

摘要

目的综述

本文旨在描述内皮细胞在高血压和血脂异常发展中的作用,并指出有前途的治疗方向。

最近的发现

血脂异常可能促进高血压的发展,而这两种“沉默杀手”的协同作用会增加动脉粥样硬化的风险。高血压和血脂异常的共同病理生理基础是内皮细胞功能障碍,其表现为内稳态、氧化还原平衡、血管张力、炎症和血栓形成的失调。针对这些过程中作用的介质的治疗可能具有开创性。对高血压和血脂异常的代谢组学研究揭示了新的治疗靶点。将访谈、临床检查、创新成像和组学特征与人工智能相结合的最先进解决方案已被证明可改善患者的风险分层和治疗效果。高血压和血脂异常的发病机制发生在血管内皮细胞。涉及内皮细胞生物标志物和生物信息学进展的新方法可能为患者管理开辟新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4328/10471742/76a6cf6651ba/11883_2023_1132_Fig1_HTML.jpg

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