AIM2 (Absent In Melanoma 2)

Aggressive LDL lowering reverses inflammasome activation and induces pro-resolving changes in macrophages in Jak2VF MPN, halting atherosclerosis progression and promoting features of plaque stabilization. These findings suggest that aggressive LDL cholesterol lowering could reverse atherosclerotic cardiovascular disease (ACVD) risk in individuals with JAK2VF CHIP or MPN.

Using both clinical samples and experimental models, we demonstrate that the cell-permeable derivative dimethyl-α-ketoglutarate (DM-α-KG) exacerbates lipopolysaccharide (LPS)-induced tissue injury and cell death, whereas isocitrate dehydrogenase (IDH1) inhibition (IDH-305) or genetic ablation reduces α-KG levels and confers protection...These findings establish α-KG as a critical immunometabolic checkpoint in sepsis that licenses inflammatory cell death via TET2-mediated epigenetic control of AIM2. Our work not only elucidates a novel α-KG/TET2/AIM2 signaling axis in sepsis pathogenesis but also highlights the therapeutic potential of targeting this pathway to modulate immune responses.

This study demonstrates that GLA exerts neuroprotective effects by activating the Nrf2/HO-1 antioxidant pathway and inhibiting AIM2 inflammasome-mediated pyroptosis. These findings suggest that GLA is a candidate drug with multi-target therapeutic potential, likely possessing clinical value for the treatment of SCI.

A novel pathway by which serum type-I IFN propagates innate immune dysfunction in SLE via the STAT1-STAT2/AIM2 inflammasome axis in monocytes has been revealed.

In summary, multimodal MRI enables dynamic monitoring of IP after CIRI in vivo and effectively evaluates the neuroprotective effects of Mel on IP. Mel broadens the time window for CIRI rescue and exerts a neuroprotective effect by downregulating AIM2 expression in neurons, thereby suppressing PANoptotic neuronal death in the IP areas and alleviating brain injury in rats with CIRI.

Such tools provide an important first step in identifying novel mediators of disease pathogenesis and likely hold the key for the discovery of potential treatment targets for BKPyVAN in the future.

This mechanism further exacerbates interstitial fibrosis by promoting the paracrine secretion of interleukin-6 and transforming growth factor-beta, which induces epithelial-mesenchymal transition (EMT) in adjacent tubular cells. These findings represent the first demonstration of the TNF-α/STAT1/AIM2 axis in triggering PANoptosis and its downstream EMT-fibrosis cascade, offering novel therapeutic targets for CAD intervention.

This study provides the first evidence implicating XN can improve OVA-induced allergic asthma by suppressing AIM2 inflammasome activation, highlighting XN as a promising therapeutic candidate for allergic asthma.

IRF4 knockdown in LUAD cells suppressed M2 macrophage polarization, but simultaneous overexpression of AIM2 restored it to baseline levels. IRF4 drives M2 macrophage polarization in LUAD via the AIM2-mediated PI3K/AKT signaling pathway.

Here, we review the current evidence on AIM2 inflammasome involvement in AS pathogenesis and its potential as a therapeutic target. This approach offers new insight into disease control through re-establishing the balance between mitochondrial dysfunction and autoimmunity.

Furthermore, TFRC knockdown effectively reduced the levels of these genes. In conclusion, TFRC facilitates PANoptosis in TC, potentially through interactions with genes such as CD34, LDHA and LDLR.