ReviewMetabolism open2026
Endoplasmic reticulum stress and organelle crosstalk: Core mechanisms and therapeutic targets in diabetic kidney disease.
Review in Metabolism open, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Diabetic kidney disease (DKD) remains the leading global cause of end-stage renal disease, with persistent residual renal damage even after standard clinical interventions including SGLT2 inhibitors and GLP-1 receptor agonists. Accumulating preclinical evidence indicates that sustained endoplasmic reticulum (ER) dysfunction may act as an important integrating mechanism contributing to renal cellular injury in DKD, beyond its canonical function in protein folding, although direct clinical evidence in human DKD remains limited. This review examines how interacting diabetic metabolic and inflammatory stressors, including glucotoxicity, lipotoxicity, advanced glycation end products, and chronic inflammation, disrupt ER homeostasis and promote persistent ER stress. Long-term ER perturbation induces a pathogenic shift of the unfolded protein response (UPR) from adaptive homeostasis maintenance toward pro-apoptotic and pro-inflammatory signaling, alongside disordered lipid biosynthesis and Ca
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