Pyroptosis: An Accomplice in the Induction of Multisystem Complications Triggered by Obstructive Sleep Apnea

Abstract

Obstructive sleep apnea (OSA) is a common respiratory disorder, primarily characterized by two pathological features: chronic intermittent hypoxia (CIH) and sleep deprivation (SD). OSA has been identified as a risk factor for numerous diseases, and the inflammatory response related to programmed cell necrosis is believed to play a significant role in the occurrence and progression of multisystem damage induced by OSA, with increasing attention being paid to pyroptosis. Recent studies have indicated that OSA can elevate oxidative stress levels in the body, activating the process of pyroptosis within different tissues, ultimately accelerating organ dysfunction. However, the molecular mechanisms of pyroptosis in the multisystem damage induced by OSA remain unclear. Therefore, this review focuses on four major systems that have received concentrated attention in existing research in order to explore the role of pyroptosis in promoting renal diseases, cardiovascular diseases, neurocognitive diseases, and skin diseases in OSA patients. Furthermore, we provide a comprehensive overview of methods for inhibiting pyroptosis at different molecular levels, with the goal of identifying viable targets and therapeutic strategies for addressing OSA-related complications.

Keywords: NLRP3 inflammasome; chronic intermittent hypoxia; obstructive sleep apnea; pyroptosis; sleep deprivation.

Figure 1

Mechanisms of pyroptosis.

Figure 2

OSA promotes systemic complications through pyroptosis.

Figure 3

Mechanisms and targets for inhibiting pyroptosis in OSA patients. CPAP and SalB: inhibit ROS release. BCA, ATO, API, Sal, SalB, KAE: inhibit the NF-κB/NLRP3 axis activation. DMF, NU6300: inhibit the cleavage of GSDMD. DSF, NSA: prevent the membrane translocation of GSDMD-NT. MFE, BA, SL, semaglutide: downregulate the levels of miR-155. The red arrow represents the inhibitory effect of the molecules.