NLRP3 inflammasome as a potential treatment in ischemic stroke concomitant with diabetes

The NLRP3 (nucleotide-binding oligomerization domain-like receptor [NLR] family pyrin domain-containing 3) inflammasome is a member of the NLR family of innate immune cell sensors. These are crucial regulators of cytokine secretions, which promote ischemic cell death and insulin resistance. This rev...

Full description

Saved in:
Bibliographic Details
Published inJournal of neuroinflammation Vol. 16; no. 1; p. 121
Main Authors Hong, Pu, Gu, Ruo-Nan, Li, Feng-Xian, Xiong, Xiao-Xing, Liang, Wen-Bin, You, Zhi-Jian, Zhang, Hong-Fei
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 07.06.2019
BioMed Central
BMC
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The NLRP3 (nucleotide-binding oligomerization domain-like receptor [NLR] family pyrin domain-containing 3) inflammasome is a member of the NLR family of innate immune cell sensors. These are crucial regulators of cytokine secretions, which promote ischemic cell death and insulin resistance. This review summarizes recent progress regarding the NLRP3 inflammasome as a potential treatment for ischemic stroke in patients with diabetes, two complicated diseases that often occur together. Stroke worsens glucose metabolism abnormalities, and the outcomes after stroke are more serious for diabetic patients compared with those without diabetes. Inflammation contributes to organ injury after ischemic stroke and diabetes. Recent research has focused on inhibiting the activation of inflammasomes and thus reducing the maturation of proinflammatory cytokines such as interleukin (IL)-1β and IL-18. Studies suggest that inhibition of NLRP3 prevents or alleviates both ischemic stroke and diabetes. Targeting against the assembly and activity of the NLRP3 inflammasome is a potential and novel therapy for inflammasome-associated diseases, including ischemic stroke concomitant with diabetes.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:1742-2094
1742-2094
DOI:10.1186/s12974-019-1498-0