ArticleCell biochemistry and biophysics2026
dsDNA-Induced AIM2 Pyroptosis in Glomerular Endothelial Cells Aggravate Lupus Nephritis.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The mechanism of how double-stranded DNA (dsDNA) contributes to Lupus nephritis (LN) remains undefined. The cytoplasmic DNA receptor, absent in melanoma 2 (AIM2) initiates inflammasome complex formation, facilitating gasdermin D (GSDMD) degradation and triggering pyroptosis in response to cytosolic DNA. In this study, we aimed to explore how AIM2 deficiency influences LN in a mouse model predisposed to lupus. The level of dsDNA in serum of healthy individuals and SLE patients were detected. Next in vivo, pristane-induced lupus (PIL) models were established in AIM2 knockdown (AIM2-/-) mice and wild type (WT) mice. Proteinuria, complement C3, IgG, kidney histopathology, expression of mesangial cells and endothelial cells in kidney, and GSDMD expression were tested. Subsequently, human umbilical vein endothelial cells (HUVECs) were cultivated in vitro and treated with dsDNA stimulation. Following this, we examined lactate dehydrogenase (LDH) release and assessed the expression levels of AIM2, caspase-1, and GSDMD. Levels of dsDNA were elevated in patients with systemic lupus erythematosus (SLE) relative to healthy controls. Additionally, AIM2 expression within the kidneys of PIL mice demonstrated increased expression compared to WT-Vehicle counterparts. Next in vivo we identified that AIM2 knockdown ameliorated proteinuria, complement C3 and IgG level, and renal damage in PIL mice. Interestingly, we found a decrease of the number of endothelial cells but not mesangial cells, and an increase of GSDMD expression in the glomeruli of PIL WT mice, and AIM2 knockdown restored the number of glomerular endothelial cells and reduced GSDMD expression in lupus mice. In addition, we investigated the damage to lungs and spleen in lupus mice after blocking AIM2. the data revealed AIM2-deficiency ameliorated inflammation in the lungs and reduced structural changes in the spleen. In vitro, dsDNA stimulated HUVECs showed an increase of LDH release, and aslo the expression of AIM2, caspase-1 and GSDMD were significant elevated. These results demonstrated that AIM2-deficiency reduced renal injury of PIL mice, which may be related to the inhibitory effect on DNA induced glomerular endothelial cell pyroptosis. Furthermore, AIM2 knockdown protected mice with lupus from damage to other organs. Overall, our study provided a new therapeutic direction in LN.
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