Canonical and non-canonical effects of the NLRP3 inflammasome in kidney inflammation and fibrosis
G Lorenz, MN Darisipudi… - Nephrology Dialysis …, 2014 - academic.oup.com
G Lorenz, MN Darisipudi, HJ Anders
Nephrology Dialysis Transplantation, 2014•academic.oup.comNLRP-3 inflammasome is one of several intracellular danger recognition platforms that
integrates infectious or non-infectious types of danger into the expression of pro-
inflammatory cytokines to set-up inflammation for danger control. NLRP3 activation induces
three types of caspase-1-mediated responses: secretion of IL-1beta, secretion of IL-18 and a
programmed form of cell death, referred to as pyroptosis. Similar to the well-documented
impact of Toll-like receptor-driven danger signalling in kidney disease, evolving data now …
integrates infectious or non-infectious types of danger into the expression of pro-
inflammatory cytokines to set-up inflammation for danger control. NLRP3 activation induces
three types of caspase-1-mediated responses: secretion of IL-1beta, secretion of IL-18 and a
programmed form of cell death, referred to as pyroptosis. Similar to the well-documented
impact of Toll-like receptor-driven danger signalling in kidney disease, evolving data now …
Abstract
NLRP-3 inflammasome is one of several intracellular danger recognition platforms that integrates infectious or non-infectious types of danger into the expression of pro-inflammatory cytokines to set-up inflammation for danger control. NLRP3 activation induces three types of caspase-1-mediated responses: secretion of IL-1beta, secretion of IL-18 and a programmed form of cell death, referred to as pyroptosis. Similar to the well-documented impact of Toll-like receptor-driven danger signalling in kidney disease, evolving data now suggest a similar involvement of the NLRP3 inflammasome in renal inflammation. Here, we discuss the accumulating data on NLRP3 in the kidney: its IL-1beta and IL-18-dependent ‘canonical’ effects and the current evidence for its ‘non-canonical’ effects, e.g. in tumor growth factor (TGF)-beta signalling, epithelial-mesenchymal transition and fibrosis. Research in this area will certainly uncover yet unknown aspects of danger signalling in the kidney and how it drives renal inflammation and immunopathology.
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