Department of Medicine - DIMED, University of Padova, Padova, Italy.
Molecular Internal Medicine, University of Zürich, Zürich, Switzerland.
J Hypertens. 2018 Mar;36(3):451-461. doi: 10.1097/HJH.0000000000001599.
: Kidney damage is a common consequence of arterial hypertension, but is also a cause of atherogenesis. Dysfunction and/or harm of the endothelium in glomeruli and tubular interstitium damage the function of these structures and translates into dynamic changes of filtration fraction, with progressive reduction in glomerular filtration rate, expansion of extracellular fluid volume, abnormal ion balance, and hypoxia, ultimately leading to chronic kidney disease. Considering the key role played by endothelial dysfunction in chronic kidney disease, the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension and the Japanese Society of Hypertension have critically reviewed available knowledge on the mechanisms underlying endothelial cell injury. This resulted into two articles: in the first, we herein examine the mechanisms by which endothelial factors induce vascular remodeling and the role of different players, including endothelin-1, the renin-angiotensin-aldosterone system and their interactions, and of oxidative stress; in the second, we discuss the role of endothelial dysfunction in the major disease conditions that affect the kidney.
肾脏损伤是动脉高血压的常见后果,但也是动脉粥样硬化形成的原因。肾小球和肾小管间质内皮功能障碍和/或损伤会破坏这些结构的功能,并导致滤过分数的动态变化,肾小球滤过率逐渐降低,细胞外液容量扩张,离子平衡异常和缺氧,最终导致慢性肾脏病。考虑到内皮功能障碍在慢性肾脏病中的关键作用,欧洲高血压学会和日本高血压学会的内皮素和内皮因子工作组对内皮细胞损伤的潜在机制进行了批判性回顾。这导致了两篇文章:第一篇中,我们在此检查了内皮因子诱导血管重塑的机制以及不同参与者(包括内皮素 1、肾素-血管紧张素-醛固酮系统及其相互作用以及氧化应激)的作用;第二篇中,我们讨论了内皮功能障碍在影响肾脏的主要疾病状况中的作用。
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