Podocyte biology and pathogenesis of kidney disease.

Podocyte biology and pathogenesis of kidney disease.
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DOI:
10.1146/annurev-med-050311-163340
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发表时间:
2013
影响因子:
10.5
通讯作者:
Sever S
Sever S
中科院分区:
医学1区
文献类型:
--
作者:
Reiser J;Sever S

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蛋白尿性慢性肾病(CKD)曾经是一种罕见的疾病,被认为主要是由基因突变引起的,但现已成为一种全球流行病,严重降低了数百万人的生活质量。尽管 CKD 的面貌发生了变化,但治疗方案和资源仍然严重过时,并且未能阻止或逆转肾脏相关疾病的影响。组织学和遗传数据强烈暗示了一个有希望的目标:足细胞。足细胞是肾小球的终末分化细胞,对于肾过滤器的完整性至关重要。它们的功能主要基于其复杂的结构,其中包括足突。这些肌动蛋白驱动的膜延伸的丧失与尿液中蛋白质的存在、足细胞的丧失、慢性肾病的发展以及最终的肾衰竭密切相关。
Proteinuric chronic kidney disease (CKD), once a rare affliction believed to be mainly caused by genetic mutations, has become a global pandemic that severely diminishes the quality of life for millions. Despite the changing face of CKD, treatment options and resources remain woefully antiquated and have failed to arrest or reverse the effects of kidney-related diseases. Histological and genetic data strongly implicate one promising target: the podocyte. Podocytes are terminally differentiated cells of the kidney glomerulus that are essential for the integrity of the kidney filter. Their function is primarily based on their intricate structure, which includes foot processes. Loss of these actin-driven membrane extensions is tightly connected to the presence of protein in the urine, podocyte loss, development of CKD, and ultimately renal failure.
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