Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy

The incidence of chronic kidney disease (CKD) has been rising yearly. And it has become one of the major hazards to public health in the world. The underlying causes of CKD include primary/secondary glomerulonephritis, diabetic nephropathy, hypertensive renal damage, renal tubulointerstitial lesions...

Full description

Saved in:
Bibliographic Details
Main Authors: Deng Xuan, Wang Yu
Format: Article
Language:zho
Published: Editorial Department of Journal of Clinical Nephrology 2022-07-01
Series:Linchuang shenzangbing zazhi
Subjects:
Online Access:http://www.lcszb.com/thesisDetails#10.3969/j.issn.1671-2390.2022.07.011
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849312258763522048
author Deng Xuan
Wang Yu
author_facet Deng Xuan
Wang Yu
author_sort Deng Xuan
collection DOAJ
description The incidence of chronic kidney disease (CKD) has been rising yearly. And it has become one of the major hazards to public health in the world. The underlying causes of CKD include primary/secondary glomerulonephritis, diabetic nephropathy, hypertensive renal damage, renal tubulointerstitial lesions and genetic disorder, etc. Diabetic kidney disease (DKD), one of the causes of CKD, is a complication of diabetic renal microangiopathy and end-stage renal disease ensues if left unchecked. The specific pathogenesis of DKD has remained elusive. Hyperglycemia causes immune-mediated inflammation and renal injuries. However, immune-mediated inflammatory factors are one of the important causes of DKD. During hyperglycemia, such inflammatory response cells as interleukin and tumor necrosis factors are mobilized to infiltrate kidney and stimulate the development of renal microangiopathy through a large variety of signaling pathways. In recent years, Toll-like receptor 4 (TLR4) and NoD-like receptor family pyrin domain-containing protein 3 (NLRP3) play an important role in renal-related immune inflammatory diseases. And TLR4/NLRP3 inflammatory bodies are closely correlated with the pathogenesis of DKD. Elevated TLR4 level has been detected under hyperglycemia. However, TLR4 stimulates the maturation and release of downstream inflammatory factors by activating NF-κB through recognizing specific ligands and NLRP3 inflammatory bodies exist sparsely in mesangial cells of DKD. The activation of NF-κB activates the assembly and maturation of inflammatory bodies, thus promoting the release of inflammatory cytokines. Thus TLR4 and NLRP3 play some important roles in the development of diabetic nephropathy.
format Article
id doaj-art-a972ec86c8424bed8edcd67aeb3d6905
institution Kabale University
issn 1671-2390
language zho
publishDate 2022-07-01
publisher Editorial Department of Journal of Clinical Nephrology
record_format Article
series Linchuang shenzangbing zazhi
spelling doaj-art-a972ec86c8424bed8edcd67aeb3d69052025-08-20T03:53:07ZzhoEditorial Department of Journal of Clinical NephrologyLinchuang shenzangbing zazhi1671-23902022-07-012259560128887562Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathyDeng XuanWang YuThe incidence of chronic kidney disease (CKD) has been rising yearly. And it has become one of the major hazards to public health in the world. The underlying causes of CKD include primary/secondary glomerulonephritis, diabetic nephropathy, hypertensive renal damage, renal tubulointerstitial lesions and genetic disorder, etc. Diabetic kidney disease (DKD), one of the causes of CKD, is a complication of diabetic renal microangiopathy and end-stage renal disease ensues if left unchecked. The specific pathogenesis of DKD has remained elusive. Hyperglycemia causes immune-mediated inflammation and renal injuries. However, immune-mediated inflammatory factors are one of the important causes of DKD. During hyperglycemia, such inflammatory response cells as interleukin and tumor necrosis factors are mobilized to infiltrate kidney and stimulate the development of renal microangiopathy through a large variety of signaling pathways. In recent years, Toll-like receptor 4 (TLR4) and NoD-like receptor family pyrin domain-containing protein 3 (NLRP3) play an important role in renal-related immune inflammatory diseases. And TLR4/NLRP3 inflammatory bodies are closely correlated with the pathogenesis of DKD. Elevated TLR4 level has been detected under hyperglycemia. However, TLR4 stimulates the maturation and release of downstream inflammatory factors by activating NF-κB through recognizing specific ligands and NLRP3 inflammatory bodies exist sparsely in mesangial cells of DKD. The activation of NF-κB activates the assembly and maturation of inflammatory bodies, thus promoting the release of inflammatory cytokines. Thus TLR4 and NLRP3 play some important roles in the development of diabetic nephropathy.http://www.lcszb.com/thesisDetails#10.3969/j.issn.1671-2390.2022.07.011Chronic kidney diseaseDiabetic kidney diseaseToll-Like Receptor 4Nod-like receptor family pyrin domain-containing protein 3
spellingShingle Deng Xuan
Wang Yu
Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy
Linchuang shenzangbing zazhi
Chronic kidney disease
Diabetic kidney disease
Toll-Like Receptor 4
Nod-like receptor family pyrin domain-containing protein 3
title Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy
title_full Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy
title_fullStr Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy
title_full_unstemmed Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy
title_short Research advances of role of TLR4/NLRP3 inflammasome in diabetic nephropathy
title_sort research advances of role of tlr4 nlrp3 inflammasome in diabetic nephropathy
topic Chronic kidney disease
Diabetic kidney disease
Toll-Like Receptor 4
Nod-like receptor family pyrin domain-containing protein 3
url http://www.lcszb.com/thesisDetails#10.3969/j.issn.1671-2390.2022.07.011
work_keys_str_mv AT dengxuan researchadvancesofroleoftlr4nlrp3inflammasomeindiabeticnephropathy
AT wangyu researchadvancesofroleoftlr4nlrp3inflammasomeindiabeticnephropathy