Inflammasome activation in podocytes: a new mechanism of glomerular diseases

Inflammasome activation in podocytes: a new mechanism of glomerular diseases
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足细胞炎症小体激活:肾小球疾病的新机制

DOI:
10.1007/s00011-020-01354-w
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发表时间:
2020-05
期刊:
Inflamm Res
影响因子:
--
通讯作者:
Zhang C(通讯作者)
Zhang C(通讯作者)
中科院分区:
其他
文献类型:
--
作者:
Xiong W;Meng X(通讯作者);Zhang C(通讯作者)

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简介炎症小体是一种多蛋白复合物,是先天免疫的重要组成部分。它主要由三部分组成,含有caspase募集结构域(ASC)的凋亡相关斑点样蛋白、caspase蛋白酶和NOD样受体(NLR)家族蛋白(如NLRP1)或HIN200家族蛋白(如AIM2)。炎症小体在许多自身免疫性疾病和慢性炎症反应中被广泛研究,例如家族性周期性自身炎症反应、2型糖尿病、阿尔茨海默病和动脉粥样硬化。肾脏炎症小体的激活在肾小球和肾小管间质疾病中已被广泛报道。足细胞在维持肾小球滤过屏障的正常结构和功能中发挥着关键作用。最近,研究表明,足细胞作为一组肾脏驻留细胞,可以表达NLRP3炎症小体的所有必需成分,NLRP3炎症小体被激活并促进局部肾脏的炎症反应。方法通过文献回顾,进一步总结不同疾病条件下足细胞NLRP3炎症小体激活的现有证据和相关分子机制。结果足细胞是肾小球滤过屏障的关键组成部分,足细胞再生丧失是肾小球滤过屏障的主要限制因素。蛋白尿恢复。通过对足细胞炎症小体进行更全面的研究,将为肾脏疾病的治疗提供新的靶点和可能性。
IntroductionInflammasome is a multi-protein complex which is an important constituent of innate immunity. It mainly consists of three parts, apoptosis-associated speck-like protein containing caspase recruitment domain (ASC), caspase protease, and a NOD-like receptor (NLR) family protein (such as NLRP1) or an HIN200 family protein (such as AIM2). Inflammasome is widely studied in many autoimmune diseases and chronic inflammatory reactions, such as familial periodic autoinflammatory response, type 2 diabetes, Alzheimer's disease, and atherosclerosis. Activation of inflammasome in the kidney has been widely reported in glomerular and tubular-interstitial diseases. Podocytes play a critical role in maintaining the normal structure and function of glomerular filtration barrier. Recently, it has been demonstrated that podocytes, as a group of renal residential cells, can express all necessary components of NLRP3 inflammasome, which is activated and contribute to inflammatory response in the local kidney.MethodsLiterature review was conducted to further summarize current evidence of podocyte NLRP3 inflammasome activation and related molecular mechanisms under different disease conditions.ResultsPodocytes are a key component of the glomerular filtration barrier, and the loss of podocyte regeneration is a major limiting factor in the recovery of proteinuria. Through a more comprehensive study of inflammasome in podocytes, it will provide new targets and possibilities for the treatment of kidney diseases.
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