The role played by perivascular cells in kidney interstitial injury.
The role played by perivascular cells in kidney interstitial injury.
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DOI：
10.5414/cn107371
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发表时间：
2012-05
影响因子：
1.1
通讯作者：
Duffield JS
中科院分区：
文献类型：
--
作者：
Rojas A;Chang FC;Lin SL;Duffield JS
肾脏纤维化是一种影响全世界数百万人的疾病，并且是导致器官衰竭的器官功能进行性丧失的预兆。最近的研究结果表明，了解纤维化的发展和进展机制将导致迫切需要新的治疗方法来抵消器官功能的丧失。最近，鲜为人知的细胞，内衬肾脏微血管，称为周细胞，被确定为前体细胞，成为瘢痕形成肌成纤维细胞。肾周细胞是位于毛细血管壁中的广泛分支的细胞，嵌入微血管基底膜内，并且不完全地包被内皮细胞，它们与内皮细胞建立局灶性接触。作为对肾损伤的响应，周细胞从内皮细胞分离并迁移到间质空间中，在那里它们经历转变成肌成纤维细胞。脱离导致纤维化，但也留下不稳定的内皮，易于稀疏。血管内皮生长因子受体和血小板衍生生长因子受体对损伤的反应中的内皮-周细胞串扰已被确定为治疗干预的主要新靶点。
Fibrosis of the kidney is a disease affecting millions worldwide and is a harbinger of progressive loss of organ function resulting in organ failure. Recent findings suggest that understanding mechanisms of development and progression of fibrosis will lead to new therapies urgently required to counteract loss of organ function. Recently, little-known cells that line the kidney microvasculature, known as pericytes, were identified as the precursor cells which become the scar-forming myofibroblasts. Kidney pericytes are extensively branched cells located in the wall of capillaries, embedded within the microvascular basement membrane, and incompletely envelope endothelial cells with which they establish focal contacts. In response to kidney injuries, pericytes detach from endothelial cells and migrate into the interstitial space where they undergo a transition into myofibroblasts. Detachment leads to fibrosis but also leaves an unstable endothelium, prone to rarefaction. Endothelial-pericyte crosstalk at the vascular endothelial growth factor receptors and platelet derived growth factor receptors in response to injury have been identified as major new targets for therapeutic intervention.
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