ArticleActa diabetologica2026
Myeloid myeloid PRDM16 restrains macrophage inflammatory remodeling and renal fibrosis in diabetic kidney disease by limiting PI3K/AKT activation.
Article in Acta diabetologica, 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
backgroundDiabetic kidney disease (DKD) is driven by persistent metabolic stress, immune dysregulation and progressive renal fibrosis. PRDM16 is a metabolic transcriptional regulator involved in adipose remodeling, mitochondrial activity and tissue homeostasis, but whether myeloid PRDM16 links diabetic metabolic stress to macrophage polarization and renal fibrosis remains unclear.
methodsPublic DKD transcriptomic datasets were analyzed to identify PRDM16-associated immune and macrophage signatures. Myeloid PRDM16-deficient mice and littermate controls were used to establish experimental DKD. Renal injury, fibrotic remodeling, macrophage polarization and PI3K/AKT signaling were evaluated by histological staining, immunostaining, ELISA, qRT-PCR and western blotting. High glucose-stimulated BMDMs and THP-1-derived macrophages were used for mechanistic validation, and LY294002 was applied to inhibit PI3K/AKT signaling.
resultsBioinformatic analysis linked PRDM16 expression with macrophage-related immune features in DKD. In vivo, myeloid PRDM16 deficiency aggravated renal matrix accumulation, collagen deposition and α-SMA/Collagen-I expression. PRDM16 loss promoted a shift from M2-like macrophages toward M1-like inflammatory macrophages, characterized by increased CD80, CD86, NOS2, TNF-α and IL-1β, together with reduced CD206, Arg1, Fizz1, IL-10 and IL-4. Mechanistically, PRDM16 deficiency enhanced PI3K/AKT phosphorylation in macrophages, whereas LY294002 partially reversed M1-like polarization and attenuated renal inflammation and fibrosis.
conclusionMyeloid PRDM16 acts as a metabolic-immune regulator that restrains M2-to-M1 macrophage polarization and limits renal fibrotic progression in DKD. Loss of PRDM16 aggravates macrophage-driven inflammation and fibrosis partly through PI3K/AKT activation, suggesting that the PRDM16-PI3K/AKT axis may represent a potential target for macrophage-directed intervention in diabetic kidney disease.
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