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NLRP3炎症小体与特发性膜性肾病的相关性研究
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Abstract:
特发性膜性肾病(IMN)是一种自身免疫性疾病，是肾病综合征的主要原因之一，由自身抗体攻击足细胞抗原导致原位产生免疫复合物而引起，该疾病表现出异质性的结果，大约30%的病例进展为终末期肾病。NLRP3炎性小体是一种细胞内多蛋白复合物，作为先天免疫系统中的重要传感器，NLRP3检测外源性致病性侵袭和内源性细胞损伤，并通过形成NLRP3炎性小体(一种激活caspase-1的超分子复合物)来做出反应。越来越多的证据表明，特发性膜性肾病的发病与NLRP3炎症小体有关。抑制NLRP3炎性小体为治疗特发性膜性肾病提供了更多的可能性。
Idiopathic membranous nephropathy (IMN) is an autoimmune disease and one of the main causes of nephrotic syndrome. It is caused by the in-situ formation of immune complexes resulting from the attack of autoantibodies on podocyte antigens. This disease shows heterogeneous outcomes, and approximately 30% of cases progress to end-stage renal disease. The NLRP3 inflammasome is an intracellular multi-protein complex. As an important sensor in the innate immune system, NLRP3 detects exogenous pathogenic invasions and endogenous cell damage and responds by forming the NLRP3 inflammasome, a supramolecular complex that activates caspase-1. There is increasing evidence suggesting that the onset of idiopathic membranous nephropathy is related to the NLRP3 inflammasome. Inhibiting the NLRP3 inflammasome provides more possibilities for the treatment of idiopathic membranous nephropathy.
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