The Crosstalk between Nrf2 and Inflammasomes

International Journal of Molecular Sciences

卷:19

Martha Garstkiewicz¹  Paulina Hennig¹  Michela Di Filippo¹  Hans-Dietmar Beer¹  Serena Grossi¹  Lars E. French¹ 

[1] Department of Dermatology, University Hospital of Zurich, Gloriastrasse 31, F30, CH-8091 Zurich, Switzerland;

关键词: caspase-1;    Nrf2;    inflammasome;    nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3);    inflammation;   

DOI  :  10.3390/ijms19020562

来源: DOAJ

【 摘 要 】

The Nrf2 (nuclear factor E2-related factor or nuclear factor (erythroid-derived 2)-like 2) transcription factor is a key player in cytoprotection and activated in stress conditions caused by reactive oxygen species (ROS) or electrophiles. Inflammasomes represent central regulators of inflammation. Upon detection of various stress factors, assembly of the inflamasome protein complex results in activation and secretion of proinflammatory cytokines. In addition, inflammasome activation causes pyroptosis, a lytic form of cell death, which supports inflammation. There is growing evidence of a crosstalk between the Nrf2 and inflammasome pathways at different levels. For example, Nrf2 activating compounds inhibit inflammasomes and consequently inflammation. This review summarizes what is known about the complex and predominantly antagonistic relationship of both stress-activated pathways.

【 授权许可】

Unknown