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高血压中的全身及心脏微血管功能障碍

Systemic and Cardiac Microvascular Dysfunction in Hypertension.

作者信息

Durante Alessandro, Mazzapicchi Alessandro, Baiardo Redaelli Martina

机构信息

Interventional and Clinical Cardiology Unit, Policlinico San Marco, 24040 Zingonia, Italy.

Azienda Ospedaliero-Universitaria Policlinico "Sant'Orsola", University of Bologna, 40125 Bologna, Italy.

出版信息

Int J Mol Sci. 2024 Dec 11;25(24):13294. doi: 10.3390/ijms252413294.

Abstract

Hypertension exerts a profound impact on the microcirculation, causing both structural and functional alterations that contribute to systemic and organ-specific vascular damage. The microcirculation, comprising arterioles, capillaries, and venules with diameters smaller than 20 μm, plays a fundamental role in oxygen delivery, nutrient exchange, and maintaining tissue homeostasis. In the context of hypertension, microvascular remodeling and rarefaction result in reduced vessel density and elasticity, increasing vascular resistance and driving end-organ damage. The pathophysiological mechanisms underlying hypertensive microvascular dysfunction include endothelial dysfunction, oxidative stress, and excessive collagen deposition. These changes impair nitric oxide (NO) bioavailability, increase reactive oxygen species (ROS) production, and promote inflammation and fibrosis. These processes lead to progressive vascular stiffening and dysfunction, with significant implications for multiple organs, including the heart, kidneys, brain, and retina. This review underscores the pivotal role of microvascular dysfunction in hypertension-related complications and highlights the importance of early detection and therapeutic interventions. Strategies aimed at optimizing blood pressure control, improving endothelial function, and targeting oxidative stress and vascular remodeling are critical to mitigating the systemic consequences of hypertensive microvascular damage and reducing the burden of related cardiovascular and renal diseases.

摘要

高血压对微循环产生深远影响,导致结构和功能改变,进而促成全身和器官特异性血管损伤。微循环由直径小于20μm的小动脉、毛细血管和小静脉组成,在氧气输送、营养物质交换及维持组织内环境稳定方面发挥着重要作用。在高血压情况下,微血管重塑和稀疏会导致血管密度和弹性降低,增加血管阻力并引发靶器官损伤。高血压性微血管功能障碍的病理生理机制包括内皮功能障碍、氧化应激和胶原蛋白过度沉积。这些变化会损害一氧化氮(NO)的生物利用度,增加活性氧(ROS)生成,并促进炎症和纤维化。这些过程会导致血管逐渐硬化和功能障碍,对包括心脏、肾脏、大脑和视网膜在内的多个器官产生重大影响。本综述强调了微血管功能障碍在高血压相关并发症中的关键作用,并突出了早期检测和治疗干预的重要性。旨在优化血压控制、改善内皮功能以及针对氧化应激和血管重塑的策略对于减轻高血压性微血管损伤的全身后果以及减轻相关心血管和肾脏疾病的负担至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a88b/11677602/c2d271e02898/ijms-25-13294-g001.jpg

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