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. 2021 Apr 7;7(15):eabe9274. doi: 10.1126/sciadv.abe9274

Fig. 8. Mechanisms whereby GAT2 deficiency lowers IL-1β production in proinflammatory macrophages.

Fig. 8

Depletion of GAT2 activates MAT2A/PNP-mediated betaine/SAM/hypoxanthine signaling through increased GAT4 expression to dampen NLRP3–ASC–caspase-1 complex formation and boost OXPHOS-related gene expression (chiefly Ndufb9) by targeting KID3 via methylation, lowering IL-1β in proinflammatory macrophages. Notably, GAT2 deficiency attenuates macrophage-mediated inflammatory responses in vivo, including LPS-induced sepsis, infection-induced pneumonia, and HFD-induced obesity.