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NLRP3 Deficiency Attenuates Renal Fibrosis and Ameliorates Mitochondrial
Dysfunction in a Mouse Unilateral Ureteral Obstruction Model of Chronic Kidney
Disease
#MMPMID28348462
Guo H
; Bi X
; Zhou P
; Zhu S
; Ding W
Mediators Inflamm
2017[]; 2017
(?): 8316560
PMID28348462
show ga
Background and Aims. The nucleotide-binding domain and leucine-rich repeat
containing PYD-3 (NLRP3) inflammasome has been implicated in the pathogenesis of
chronic kidney disease (CKD); however, its exact role in glomerular injury and
tubulointerstitial fibrosis is still undefined. The present study was performed
to identify the function of NLRP3 in modulating renal injury and fibrosis and the
potential involvement of mitochondrial dysfunction in the murine unilateral
ureteral obstruction (UUO) model of CKD. Methods. Employing wild-type (WT) and
NLRP3(-/-) mice with or without UUO, we evaluated renal structure, tissue injury,
and mitochondrial ultrastructure, as well as expression of some vital molecules
involved in the progression of fibrosis, apoptosis, inflammation, and
mitochondrial dysfunction. Results. The severe glomerular injury and
tubulointerstitial fibrosis induced in WT mice by UUO was markedly attenuated in
NLRP3(-/-) mice as evidenced by blockade of extracellular matrix deposition,
decreased cell apoptosis, and phenotypic alterations. Moreover, NLRP3 deletion
reversed UUO-induced impairment of mitochondrial morphology and function.
Conclusions. NLRP3 deletion ameliorates mitochondrial dysfunction and alleviates
renal fibrosis in a murine UUO model of CKD.
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