The Role of the Interplay Between Autophagy and NLRP3 Inflammasome in Metabolic Disorders

Abstract

Autophagy is an important and conserved cellular pathway in which cells transmit cytoplasmic contents to lysosomes for degradation. It plays an important role in maintaining the balance of cell composition synthesis, decomposition and reuse, and participates in a variety of physiological and pathological processes. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome can induce the maturation and secretion of Interleukin-1 beta (IL-1β) and IL-18 by activating caspase-1. It is involved in many diseases. In recent years, the interplay between autophagy and NLRP3 inflammasome has been reported to contribute to many diseases including metabolic disorders related diseases. In this review, we summarized the recent studies on the interplay between autophagy and NLRP3 inflammasome in metabolic disorders to provide ideas for the relevant basic research in the future.

The Role of Hydrogen Sulfide Regulation of Autophagy in Liver Disorders

“…In recent years, the interaction between autophagy and NLRP3 inflammasome has been reported to be involved in many metabolic disorder-related diseases, including NAFLD [ 8 ]. Moreover, NLRP3 inflammasome can be used as a target of H 2 S regulation in many diseases [ 21 ].…”

“…It is well-known that autophagy is induced by various environmental stresses, such as hypoxia, nutrient deficiency, and growth factor deficiency, so as to eliminate the damage caused by these pressures and return to normal level after stress relief [ 5 ]. Autophagy is categorized into macroautophagy, microautophagy, and chaperone-mediated autophagy according to the differences in the target specificity, inducing signal, action time, and delivery pathway to lysosomes [ 6 , 7 , 8 ]. Macroautophagy is a conservative stress response process.…”

The Complex Interplay between Autophagy and NLRP3 Inflammasome in Renal Diseases

“…Collectively, honokiol could ameliorate ASLN by inhibiting NLRP3 inflammasome activation by promoting autophagy [ 62 ]. It has been reported that ROS from damaged mitochondria can activate the NF-ĸB pathway to upregulate the transcription of NLRP3 and pro-IL-1β or to promote NLRP3 inflammasome assembly [ 63 ]. Thus, the above research indicated that the ROS/NF-ĸB pathway mediated autophagy effects on NLRP3 inflammasome.…”

Nanodiamond-Induced Thrombocytopenia in Mice Involve P-Selectin-Dependent Nlrp3 Inflammasome-Mediated Platelet Aggregation, Pyroptosis and Apoptosis

“…NLR pyrin domain containing 3 (Nlrp3) inflammasome is one of the most studied inflammasomes, sensing a variety of cellular stresses and stimulus, such as ROS, toxins, pathogens, metabolites, nucleic acids, uric acid crystals and nanoparticles ( 46 – 50 ). Several lines of evidences have implicated that over activation of inflammasomes through different pathways in cells can lead to major types of RCDs, including pyroptosis ( 47 ), apoptosis ( 51 , 52 ), necroptosis ( 52 ), ferroptosis ( 53 ) and autophagy ( 54 , 55 ). For example, inflammasome activation leads to the maturation and activation of pore-forming protein gasdermins, cell membrane rupture and cell death in pyroptosis ( 47 ).…”