The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review

Shaokai Tang; Yuanwen Geng; Yawei Wang; Qinqin Lin; Yirong Yu; Hao Li

doi:10.17305/bb.2023.9997

Authors

Shaokai Tang School of Physical Education, Yanshan University, Qinhuangdao, China
Yuanwen Geng School of Physical Education, Yanshan University, Qinhuangdao, China
Yawei Wang School of Public Administration, Yanshan University, Qinhuangdao, China
Qinqin Lin School of Physical Education, Yanshan University, Qinhuangdao, China; School of Public Administration, Yanshan University, Qinhuangdao, China
Yirong Yu School of Physical Education, Yanshan University, Qinhuangdao, China
Hao Li School of Physical Education, Yanshan University, Qinhuangdao, China

DOI:

https://doi.org/10.17305/bb.2023.9997

Keywords:

Ubiquitination, deubiquitination, NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasomes, inflammation-related diseases, post-translational modification (PTM)

Abstract

The inflammatory response is a natural immune response that prevents microbial invasion and repairs damaged tissues. However, excessive inflammatory responses can lead to various inflammation-related diseases, posing a significant threat to human health. The NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome is a vital mediator in the activation of the inflammatory cascade. Targeting the hyperactivation of the NLRP3 inflammasome may offer potential strategies for the prevention or treatment of inflammation-related diseases. It has been established that the ubiquitination and deubiquitination modifications of the NLRP3 inflammasome can provide protective effects in inflammation-related diseases. These modifications modulate several pathological processes, including excessive inflammatory responses, pyroptosis, abnormal autophagy, proliferation disorders, and oxidative stress damage. Therefore, this review discusses the regulation of NLRP3 inflammasome activation by ubiquitination and deubiquitination modifications, explores the role of these modifications in inflammation-related diseases, and examines the potential underlying mechanisms.