梗阻性肾损伤:从流体力学到分子细胞生物学。

Alvaro C Ucero, Sara Gonçalves, Alberto Benito-Martin, Beatriz Santamaría, Adrian M Ramos, Sergio Berzal, Marta Ruiz-Ortega, Jesus Egido, Alberto Ortiz
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引用次数: 4

摘要

尿路梗阻是肾脏损害的常见原因。长期以来,阻塞性肾病的生理病理一直被视为单纯的机械问题。然而,细胞和系统生物学的最新进展揭示了一个复杂的生理病理学,涉及大量的分子损伤介质,导致细胞凋亡、细胞死亡、细胞损伤导致炎症和纤维化。利用包括转基因动物在内的多种技术对输尿管梗阻动物模型进行功能研究,揭示了肾素-血管紧张素系统、转化生长因子-β1 (TGF-β1)和其他炎症介质在这一过程中的重要作用。此外,蛋白质组学和转录组学等高通量技术已经确定了可能指导临床决策的潜在生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Obstructive renal injury: from fluid mechanics to molecular cell biology.

Obstructive renal injury: from fluid mechanics to molecular cell biology.

Obstructive renal injury: from fluid mechanics to molecular cell biology.

Urinary tract obstruction is a frequent cause of renal impairment. The physiopathology of obstructive nephropathy has long been viewed as a mere mechanical problem. However, recent advances in cell and systems biology have disclosed a complex physiopathology involving a high number of molecular mediators of injury that lead to cellular processes of apoptotic cell death, cell injury leading to inflammation and resultant fibrosis. Functional studies in animal models of ureteral obstruction using a variety of techniques that include genetically modified animals have disclosed an important role for the renin-angiotensin system, transforming growth factor-β1 (TGF-β1) and other mediators of inflammation in this process. In addition, high throughput techniques such as proteomics and transcriptomics have identified potential biomarkers that may guide clinical decision-making.

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