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Defection of IFN--mediated mtDNA degradation leads to a high mitochondrial membrane potential in SLE monocytes, promoting their autoreactivity in a STING-dependent manner ( NLRP3 and AIM2 are DNA sensors that along with apoptosis-associated speck-like protein and pro-caspase-1 (component of the NLRP3 inflammasome) trigger the production of several downstream pro-inflammatory cytokines (e.g., IL-1 and IL-18) and promote pyroptosis ( Several studies have also indicated that NETs-mediate the activation of the NLRP3 inflammasome in macrophages of lupus patients, subsequently promoting IL-1 production via ROS and K + efflux ( + efflux), thereby activating the NLRP3 inflammasome ( Mitochondrial dysfunction damages organs Target organs of SLE, especially kidney, nerves, and gut, require high level of energy supply to drive their function and are more susceptible to oxidative stress and subject to chronic inflammatory injuries ( Figure 3

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