NLRP3 inflammasome: Pathogenic role and potential therapeutic target for IgA nephropathy.

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/108203

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题名:	NLRP3 inflammasome: Pathogenic role and potential therapeutic target for IgA nephropathy.
作者:	SM, Tsai YL；Tsai YL；Hua KF；Hua KF；Chen A；Chen A；Wei CW；Wei CW；Chen WS；Chen WS；Wu CY；Wu CY；Chu CL；Chu CL；余永倫；Lo CW；Lo CW；Ka SM；Ka
贡献者:	生物科技學系
日期:	2017-01
上传时间:	2017-10-30 02:43:48 (UTC+0)
摘要:	We have previously showed that IL-1β is involved in the pathogenesis of both spontaneously occurring and passively induced IgA nephropathy (IgAN) models. However, the exact causal-relationship between NLRP3 inflammasome and the pathogenesis of IgAN remains unknown. In the present study, we showed that [1] IgA immune complexes (ICs) activated NLRP3 inflammasome in macrophages involving disruption of mitochondrial integrity and induction of mitochondrial ROS, bone marrow-derived dendritic cells (BMDCs) and renal intrinsic cells; [2] knockout of NLRP3 inhibited IgA ICs-mediated activation of BMDCs and T cells; and [3] knockout of NLRP3 or a kidney-targeting delivery of shRNA of NLRP3 improved renal function and renal injury in a mouse IgAN model. These results strongly suggest that NLRP3 inflammasome serves as a key player in the pathogenesis of IgAN partly through activation of T cells and mitochondrial ROS production and that a local, kidney-targeting suppression of NLRP3 be a therapeutic strategy for IgAN.
關聯:	Scientific Reports
显示于类别:	[生物科技學系] 期刊論文

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