ArticleFrontiers in cell and developmental biology2026
Multi-omics integration identifies Acsm2/ACSM2A deficiency as a metabolic driver of ZBP1-mediated PANoptosis in acute kidney injury.
Article in Frontiers in cell and developmental biology, 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
Acute kidney injury (AKI) converges on tubular epithelial cell (TEC) death and metabolic collapse, fueling the transition to chronic kidney disease (CKD), yet the molecular link between metabolic failure and inflammatory cell death remains poorly defined. Here, we integrated cross-model transcriptomics of three mechanistically distinct murine AKI models with single-cell RNA-seq, high-dimensional weighted gene co-expression network analysis, and machine learning feature selection. This multi-omics framework identified acyl-CoA synthetase medium-chain family member 2 (Acsm2), a rate-limiting mitochondrial enzyme for medium-chain fatty acid β-oxidation, as the top conserved hub gene suppressed in injured proximal tubule cells. Acsm2/ACSM2A downregulation was confirmed in mouse AKI models and in human HK-2 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R). ACSM2A deficiency alone was sufficient to simultaneously activate apoptosis, pyroptosis, and necroptosis, indicative of PANoptosis, whereas restoration of ACSM2A expression attenuated OGD/R-induced cell death. Mechanistically,
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