PMID- 33546399
OWN - NLM
STAT- MEDLINE
DCOM- 20211101
LR  - 20211101
IS  - 2073-4409 (Electronic)
IS  - 2073-4409 (Linking)
VI  - 10
IP  - 2
DP  - 2021 Feb 3
TI  - NLRP3 Inflammasome at the Interface of Inflammation, Endothelial Dysfunction, and 
      Type 2 Diabetes.
LID - 10.3390/cells10020314 [doi]
LID - 314
AB  - Type 2 diabetes mellitus (T2DM), accounting for 90-95% cases of diabetes, is 
      characterized by chronic inflammation. The mechanisms that control inflammation 
      activation in T2DM are largely unexplored. Inflammasomes represent significant 
      sensors mediating innate immune responses. The aim of this work is to present a 
      review of links between the NLRP3 inflammasome, endothelial dysfunction, and 
      T2DM. The NLRP3 inflammasome activates caspase-1, which leads to the maturation 
      of pro-inflammatory cytokines interleukin 1beta and interleukin 18. In this review, 
      we characterize the structure and functions of NLRP3 inflammasome as well as the 
      most important mechanisms and molecules engaged in its activation. We present 
      evidence of the importance of the endothelial dysfunction as the first key step 
      to activating the inflammasome, which suggests that suppressing the NLRP3 
      inflammasome could be a new approach in depletion hyperglycemic toxicity and in 
      averting the onset of vascular complications in T2DM. We also demonstrate reports 
      showing that the expression of a few microRNAs that are also known to be involved 
      in either NLRP3 inflammasome activation or endothelial dysfunction is deregulated 
      in T2DM. Collectively, this evidence suggests that T2DM is an inflammatory 
      disease stimulated by pro-inflammatory cytokines. Finally, studies revealing the 
      role of glucose concentration in the activation of NLRP3 inflammasome are 
      analyzed. The more that is known about inflammasomes, the higher the chances to 
      create new, effective therapies for patients suffering from inflammatory 
      diseases. This may offer potential novel therapeutic perspectives in T2DM 
      prevention and treatment.
FAU - Gora, Ilona M
AU  - Gora IM
AD  - Nalecz Institute of Biocybernetics and Biomedical Engineering, Polish Academy of 
      Sciences, Ks. Trojdena 4, 02-109 Warsaw, Poland.
FAU - Ciechanowska, Anna
AU  - Ciechanowska A
AUID- ORCID: 0000-0002-8941-0166
AD  - Nalecz Institute of Biocybernetics and Biomedical Engineering, Polish Academy of 
      Sciences, Ks. Trojdena 4, 02-109 Warsaw, Poland.
FAU - Ladyzynski, Piotr
AU  - Ladyzynski P
AUID- ORCID: 0000-0003-3268-9896
AD  - Nalecz Institute of Biocybernetics and Biomedical Engineering, Polish Academy of 
      Sciences, Ks. Trojdena 4, 02-109 Warsaw, Poland.
LA  - eng
GR  - 2017/27/B/ST7/00269/National Science Centre Poland/
PT  - Journal Article
PT  - Review
DEP - 20210203
PL  - Switzerland
TA  - Cells
JT  - Cells
JID - 101600052
RN  - 0 (Inflammasomes)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
SB  - IM
MH  - Diabetes Mellitus, Type 2/*genetics/pathology
MH  - Endothelial Cells/*metabolism
MH  - Humans
MH  - Inflammasomes/*metabolism
MH  - Inflammation/*physiopathology
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism
PMC - PMC7913585
OTO - NOTNLM
OT  - NLRP3 inflammasome
OT  - endothelial cells
OT  - inflammation
OT  - type 2 diabetes mellitus
COIS- The authors declare no conflict of interest.
EDAT- 2021/02/07 06:00
MHDA- 2021/11/03 06:00
PMCR- 2021/02/03
CRDT- 2021/02/06 01:03
PHST- 2020/12/22 00:00 [received]
PHST- 2021/01/24 00:00 [revised]
PHST- 2021/01/30 00:00 [accepted]
PHST- 2021/02/06 01:03 [entrez]
PHST- 2021/02/07 06:00 [pubmed]
PHST- 2021/11/03 06:00 [medline]
PHST- 2021/02/03 00:00 [pmc-release]
AID - cells10020314 [pii]
AID - cells-10-00314 [pii]
AID - 10.3390/cells10020314 [doi]
PST - epublish
SO  - Cells. 2021 Feb 3;10(2):314. doi: 10.3390/cells10020314.