ReviewFrontiers in cell and developmental biology2026
Hyperglycaemia-induced molecular reprogramming of proximal tubular epithelial cells and its contribution to diabetic kidney disease progression-a narrative review.
Review 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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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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Abstract
Diabetic kidney disease (DKD) is the primary contributor to the development of chronic kidney disease and end-stage kidney failure globally. A hyperglycaemic microenvironment is a critical contributor of proximal tubular epithelial cell injury to disease initiation and progression. Hyperglycaemia induces profound molecular, metabolic, and structural alterations in renal tubular epithelial cells, promoting inflammation, fibrosis, and functional decline. Chronic hyperglycaemia activates multiple pathogenic pathways, including the polyol, hexosamine, protein kinase C (PKC), and advanced glycation end-product pathways, resulting in excessive reactive oxygen species generation, mitochondrial dysfunction, inflammation, and extracellular matrix accumulation. Hyperglycaemia also alters the expression of key genes, including
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