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These ROS components have a high oxidative effect on biomolecules and lead to biological damage

NLRP3 inflammasome activates caspase-1 to cleaves pro-IL-1 and pro-IL-18 into the active forms IL-1 and IL-18, meanwhile, cleaves the amino-terminal fragment of the key protein gasdermin D (GSDMD) to form N-GSDMD, which oligomerizes and forms membrane pore formation leading to pyroptosis and subsequent inflammatory response

Recent work has explored the concept of enhanced arrestins that can be potentially used to suppress excessive G protein-mediated signaling (Gurevich and Gurevich, 2020b)

The intestinal microbiota can metabolize phosphatidylcholine to trimethylamine

Mechanistically, the overexpression of GPX4 protects cells from apoptosis by detoxifying the oxidative damage of membrane lipids, inhibiting mitochondrial release of CYCS, and inactivating caspase 3 [87]