共 91 条
The Role of NLRP3 Inflammasome in Lupus Nephritis
被引:45
作者:

Oliveira, Camila Barbosa
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机构:
Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil
Univ Fed Pernambuco, Lab Immunopathol Keizo Asami LIKA, BR-50670901 Recife, PE, Brazil Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil

Lima, Camilla Albertina Dantas
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机构:
Univ Fed Pernambuco, Lab Immunopathol Keizo Asami LIKA, BR-50670901 Recife, PE, Brazil
Univ Fed Pernambuco, Dept Oceanog, BR-50670901 Recife, PE, Brazil Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil

Vajgel, Gisele
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机构:
Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil

Sandrin-Garcia, Paula
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h-index: 0
机构:
Univ Fed Pernambuco, Lab Immunopathol Keizo Asami LIKA, BR-50670901 Recife, PE, Brazil
Univ Fed Pernambuco, Dept Genet, BR-50670901 Recife, PE, Brazil Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil
机构:
[1] Univ Fed Pernambuco, Clin Hosp, Div Nephrol, BR-50670901 Recife, PE, Brazil
[2] Univ Fed Pernambuco, Lab Immunopathol Keizo Asami LIKA, BR-50670901 Recife, PE, Brazil
[3] Univ Fed Pernambuco, Dept Oceanog, BR-50670901 Recife, PE, Brazil
[4] Univ Fed Pernambuco, Dept Genet, BR-50670901 Recife, PE, Brazil
关键词:
inflammasome;
NLRP3;
lupus nephritis;
systemic lupus erythematosus;
SMALL-MOLECULE INHIBITOR;
METABOLITE COMPOUND K;
FACTOR-KAPPA-B;
DIABETIC-NEPHROPATHY;
IL-1-BETA PRODUCTION;
P2X(7) RECEPTOR;
ACTIVATION;
MURINE;
CELLS;
ERYTHEMATOSUS;
D O I:
10.3390/ijms222212476
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Lupus nephritis (LN) is the most frequent and severe of systemic lupus erythematosus (SLE) clinical manifestations and contributes to the increase of morbidity and mortality of patients due to chronic kidney disease. The NLRP3 (NLR pyrin domain containing 3) is a member of the NLR (NOD-like receptors), and its activation results in the production of pro-inflammatory cytokines, which can contribute to the pathogenesis of LN. In this review manuscript, we approach the relation between the NLRP3 inflammasome, SLE, and LN, highlighting the influence of genetic susceptibility of NLRP3 polymorphisms in the disease; the main functional studies using cellular and animal models of NLRP3 activation; and finally, some mechanisms of NLRP3 inhibition for the development of possible therapeutic drugs for LN.
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