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Department of Nephrology, Georgian American University, Tbilisi, GEO.
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View Article and Find Full Text PDFCompartment-specific adaptive responses and dysregulation under NQO1 deficiency in diabetic kidney disease: A transcriptomic GSEA-based investigation.
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Department of Nephrology, Chungnam National University, Daejeon, Republic of Korea.
Diabetic kidney disease (DKD) involves oxidative stress-driven damage to glomeruli (Gloms) and proximal convoluted tubules (PCT). NAD(P)H: quinone oxidoreductase 1 (NQO1) regulates redox balance, but its compartment-specific role remains unclear. Streptozotocin (STZ)-induced hyperglycemia increased albuminuria and foot process effacement, with NQO1 KO (NKO) mice exhibiting greater podocyte injury than WT, indicating exacerbated glomerular damage.
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Department of Pediatrics, University of Virginia, Charlottesville, VA, USA.
Primitive emunctory functions to expel harmful substances from cells and the interstitial space of multicellular organisms evolved over the past billion and a half years into the complex physiology of the metanephric kidney. Integrative biology allows empirical testing of hypotheses of the origins of renal structures from homologous single-celled precursors. Emunctory cell complexes called nephridia evolved in metazoan (cnidarian) ancestors 750 million years ago (mya).
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Ren Fail
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Department of Nephrology, China-Japan Friendship Hospital, Beijing, China.
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