TABLE 1.

Summary table of preclinical and clinical studies included in the present review study.

#	Findings	References
Preclinical studies
1	The activation of the NLRP3 inflammasome can modulate sleep induced by wakefulness. These findings show that the NLRP3 inflammasome is an important mechanism involved in sleep responses to sleep loss and pathogen components in the brain.	(Zielinski et al., 2017)
2	The biological clock regulates NLRP3 expression and activation in diverse tissues. Circadian oscillations of NLRP3 signaling is lost in clock disruption models, which contributes to the development of disorders.	(Pourcet and Duez, 2020)
3	NLRP3 inflammasomes are involved in neurovascular coupling involving SWA.	(Zielinski et al., 2020)
4	The MAPK/NLRP3 axis may be important in the development of SD neuronal pyroptosis. The NLRP3 inflammasome is thought to be a potential therapeutic target for SD-induced neuroinflammation in the hippocampus.	(Fan et al., 2021)
5	SD modifies the expression of the circadian gene Bmal1, which controls NLRP3 expression and IL-1 production. FDP’s anxiolytic effects may be mediated by inhibiting NLRP3 inflammasome activity.	(Smith et al., 2021)
6	The administration of the NLRP3 inhibitor (MCC950) prevents SD-induced changes in microglia morphology.	(Smith et al., 2019)
7	SD activates the NLRP3 inflammasome in neurons, astrocytes, and microglia, although this activation varies depending upon the brain area.	(Niznikiewicz et al., 2017)
8	Treatment with modafinil reduced inflammasome activity and neuronal pyroptosis via the NLRP3/NLRP1/NLRC4-caspase-1-IL-1β pathway. Targeting the regulation of impaired neuronal pyroptosis and neuroinflammation may be a promising therapeutic strategy for treatment of SD.	(Xiong et al., 2022)
9	The P2 × 7 receptors promote the formation of the NLRP3 inflammasome and the ATP-induced release of mature interleukin (IL)-1b and IL-18 from astrocytes, which leads to the development of chronic SD-induced depressive-like behavior.	(Xia et al., 2020)
10	Fluoxetine can prevent the activation of NLRP3 inflammasome and avoiding SD-induced neurotoxicity. Furthermore, the activation of STAT3 is an important target that regulated the expression of NLRP3 inflammasomes in an SD model.	(Xia et al., 2017)
11	This study identified the effects of rapamycin on OSA-associated renal injury. Inhibiting the mTOR signaling pathway by rapamycin can significantly reduce the levels of NLRP3 and organ damage caused by OSA.	(Liu et al., 2022)
12	MiR-224-5p reduces inflammation through the regulation of NLRP3 expression in T2DM With OSA, which finally regulated the NLRP3/IL1β pathway in the hippocampus.	(Du et al., 2020)
13	Mice lacking NLRP3 had attenuations in the significant increased amounts of NREM sleep and EEG delta power occurring 24 h after TBI and the significant reductions seen 2 months after TBI that were observed in wild-type mice. The findings suggest that NLRP3 inflammasomes contribute to dysregulated sleep occurring acutely or more persistently after TBI.	(Zielinski et al., 2021)
Clinical studies
14	Sleep fragmentation may contribute to dysregulation of NLRP3 inflammasome in IOSSD. Potential mechanisms linking sleep loss and NLRP3 inflammasome may include the activation of sympathetic system, hypothalamus-pituitary-adrenal axis and production of ROS.	(Wang et al., 2020)
15	NLRP3 inflammasome gene expression have a negative correlation with REM sleep duration. This evidence suggest that NLRP3 inflammasome is involved in the pathogenesis of the sleep disorders. inhibitors of the NLRP3 inflammasome may be promising therapeutic agents in sleep deprivation and sleep fragmentation.	(Aghelan et al., 2022)
16	There was no difference in the OSA development according to NLRP3 level.	(Kerget et al., 2021)