ArticleCurrent medical science2026
Mep1a Knockout Attenuates Unilateral Ureteral Obstruction-Induced Renal Injury by Inhibiting Glycolysis.
Article in Current medical science, 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
objectiveThis study aimed to investigate the role of Mep1a in unilateral ureteral obstruction (UUO)-induced renal injury and the underlying mechanisms.
methodsA UUO model was established in Mep1a knockout (KO) mice and wild-type littermates. Primary renal tubular epithelial cells were isolated and treated with transforming growth factor-β1 (TGF-β1), and Mep1a was knocked down by small interfering RNA. Macrophages were induced with interleukin-4 (IL-4). Renal fibrosis and pathological injury were evaluated by Masson's trichrome staining, hematoxylin-eosin (H&E) staining, and Western blotting. Glycolysis was assessed by measuring extracellular acidification rate (ECAR) and lactate production. The AKT/HIF-1α pathway was examined by Western blotting, and AKT was reactivated with SC79.
resultsMep1a was upregulated in UUO-injured kidney tissues and TGF-β1-induced renal tubular epithelial cells, but showed no significant change in IL-4-induced macrophages. Mep1a knockout mice exhibited attenuated renal fibrosis and improved renal pathological injury compared with wild-type controls after UUO. In vitro, Mep1a knockdown reduced TGF-β1-induced upregulation of Collagen I, Collagen III, α-SMA, and vimentin in renal tubular epithelial cells. Mechanistically, Mep1a deficiency suppressed glycolysis and lactate accumulation during renal injury. Mep1a deficiency also downregulated AKT phosphorylation and HIF-1α expression in TGF-β1-induced renal tubular epithelial cells, and reactivation of AKT by SC79 abolished the inhibitory effects of Mep1a deficiency on Pfkfb3, Ldha, and Pfk1 mRNA levels.
conclusionMep1a deficiency alleviates UUO-induced renal injury by inhibiting EMT via blockade of glycolysis in an HIF-1α-dependent manner.
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