PMID- 35755447
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220716
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 13
DP  - 2022
TI  - The Role of the NLRP3 Inflammasome in Mediating Glomerular and Tubular Injury in 
      Diabetic Nephropathy.
PG  - 907504
LID - 10.3389/fphys.2022.907504 [doi]
LID - 907504
AB  - The NOD-like receptor protein 3 (NLRP3) inflammasome is a multi-protein 
      signalling complex integral to the chronic inflammatory response, activated in 
      response to sterile and non-sterile cellular damage. The assembly and activation 
      of the NLRP3 inflammasome comprise a two-step process involving nuclear factor 
      kappa B (NFkB)-mediated priming, followed by canonical, non-canonical or 
      alternative signalling pathways. These result in the maturation and release of 
      inflammatory cytokines interleukin 1 beta (IL1ss) and interleukin-18 (IL18), which 
      are associated with chronic inflammatory conditions including diabetic kidney 
      disease. Diabetic nephropathy is a condition affecting  approximately 40% of people with 
      diabetes, the key underlying pathology of which is tubulointerstitial 
      inflammation and fibrosis. There is growing evidence to suggest the involvement 
      of the NLRP3 inflammasome in this chronic inflammation. Early deterioration of 
      kidney function begins in the glomerulus, with tubular inflammation dictating the 
      progression of late-stage disease. Priming and activation of the NLRP3 
      inflammasome have been linked to several clinical markers of nephropathy 
      including proteinuria and albuminuria, in addition to morphological changes 
      including mesangial expansion. Treatment options for diabetic nephropathy are 
      limited, and research that examines the impact of directly targeting the NLRP3 
      inflammasome, or associated downstream components are beginning to gain favour, 
      with several agents currently in clinical trials. This review will explore a role 
      for NLRP3 inflammasome activation and signalling in mediating inflammation in 
      diabetic nephropathy, specifically in the glomerulus and proximal tubule, before 
      briefly describing the current position of therapeutic research in this field.
CI  - Copyright (c) 2022 Williams, Cliff, Lee, Squires and Hills.
FAU - Williams, B M
AU  - Williams BM
AD  - School of Life Sciences, University of Lincoln, Lincoln, United Kingdom.
FAU - Cliff, C L
AU  - Cliff CL
AD  - School of Life Sciences, University of Lincoln, Lincoln, United Kingdom.
FAU - Lee, K
AU  - Lee K
AD  - Lincoln County Hospital, Lincoln, United Kingdom.
FAU - Squires, P E
AU  - Squires PE
AD  - School of Life Sciences, University of Lincoln, Lincoln, United Kingdom.
FAU - Hills, C E
AU  - Hills CE
AD  - School of Life Sciences, University of Lincoln, Lincoln, United Kingdom.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220609
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC9218738
OTO - NOTNLM
OT  - NLRP3
OT  - diabetes
OT  - diabetic nephropathy
OT  - fibrosis
OT  - inflammation
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/06/28 06:00
MHDA- 2022/06/28 06:01
PMCR- 2022/06/09
CRDT- 2022/06/27 03:50
PHST- 2022/03/29 00:00 [received]
PHST- 2022/05/23 00:00 [accepted]
PHST- 2022/06/27 03:50 [entrez]
PHST- 2022/06/28 06:00 [pubmed]
PHST- 2022/06/28 06:01 [medline]
PHST- 2022/06/09 00:00 [pmc-release]
AID - 907504 [pii]
AID - 10.3389/fphys.2022.907504 [doi]
PST - epublish
SO  - Front Physiol. 2022 Jun 9;13:907504. doi: 10.3389/fphys.2022.907504. eCollection 
      2022.