ArticleThe Journal of biological chemistry2026
Mrpl50 integrates glucolipotoxicity with hypoxia-inducible factor 1 alpha signaling to drive diabetic kidney disease.
Article in The Journal of biological chemistry, 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
Diabetic kidney disease (DKD), a systemic metabolic disorder, leads to renal failure and increased cardiovascular risk. A central driver of its progression is glucolipotoxicity, which triggers renal tubular injury through mechanisms that remain incompletely defined. Here, we identify Mrpl50 as a critical mediator of glucolipotoxic damage. Mrpl50 expression is upregulated under metabolic stress and correlates with DKD progression. Mrpl50 deficiency in renal tubular cell attenuated glucolipotoxic damage, while its overexpression amplified inflammatory responses. Mechanistically, Mrpl50 drives renal inflammation via the hypoxia-inducible factor 1 alpha pathway. These findings establish Mrpl50 as a molecular sensor that discriminates true hypoxia from metabolically induced pseudo-hypoxia, thereby fine-tuning the hypoxia-inducible factor 1 alpha response to govern disease progression in DKD.
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