Research Progress of Mitochondrial Mechanism in NLRP3 Inflammasome Activation and Exercise Regulation of NLRP3 Inflammasome

Abstract

NLRP3 is an important pattern recognition receptor in the innate immune system, and its activation induces a large number of pro-inflammatory cytokines, IL-1β and IL-18 which are involved in the development of various diseases. In recent years, it has been suggested that mitochondria are the platform for NLRP3 inflammasome activation. Additionally, exercise is considered as an important intervention strategy to mediate the innate immune responses. Generally, chronic moderate-intensity endurance training, resistance training and high-intensity interval training inhibit NLRP3 inflammasome activation in response to various pathological factors. In contrast, acute exercise activates NLRP3 inflammasome. However, the mechanisms by which exercise regulates NLRP3 inflammasome activation are largely unclear. Therefore, the mechanism of NLRP3 inflammasome activation is discussed mainly from the perspective of mitochondria in this review. Moreover, the effect and potential mechanism of exercise on NLRP3 inflammasome are explored, hoping to provide new target for relevant research.

Neuroprotective Effect of Dexmedetomidine against Postoperative Cognitive Decline via NLRP3 Inflammasome Signaling Pathway

“…The major aim of this study was to investigate the effect of Dex through NLRP3 signaling on a POCD model. ROS generation partly depends on the activation of NLRP3 inflammasomes [ 43 , 44 , 45 ]. We could not confirm the effect of DEX on ROS regulation in vivo.…”

“…Oxidative stress has also been proposed as the possible cause for neurodegenerative and neurocognitive diseases leading to POCD and delirium [ 46 ]. It has been reported that mitochondrial oxidative stress is one of the crucial factors involved in NLRP3 inflammasome activation [ 44 ]. It is worth investigating whether the protective effect of Dex through the NLRP3 inflammasome pathway is also related to the regulation of oxidative stress.…”

Expression of Oxidative Phosphorylation Complexes and Mitochondrial Mass in Pediatric and Adult Inflammatory Bowel Disease

“…Another possible explanation is that ROS, produced by the respiratory chain, activate the NLRP3 inflammasome, which is a known activator of excessive inflammatory responses. Under physiologic conditions there is only a low leakage of ROS, but damage to the respiratory chain produces higher amounts of ROS and stronger activation of the NLRP3 inflammasome [ 64 ]. Since it is not known, if there is an increased production of ROS within the given samples, this is only speculative.…”

Attenuation of Some Inflammatory Markers by Endurance Training in the Spinal Cord of Rats with Diabetic Neuropathic Pain

“…Accordingly, eugenol supplementation along with aerobic exercise is likely to control neuronal damage caused by diabetes [ 33 ]. It is likely that the mechanisms to explain the effects of endurance training on inflammatory factors can be attributed to the regulation of mTROS production with mitochondrial quality control (mitochondrial proliferation and mitochondrial activation), improvement of mitochondrial function, and increase in cleansing of damaged mitochondria, and hence, it can inhibit the NLRP3 inflammasome pathway and prevent extreme inflammatory reactions [ 34 ]. The nerve tissue has a frail antioxidant system, which due to high oxygen consumption is exposed to oxidative injuries; on the other hand, oxidative stress is the common pathway of cell damage as a result of hyperglycemia [ 35 ].…”