ArticleCell death & disease2023
Targeted deletion of von-Hippel-Lindau in the proximal tubule conditions the kidney against early diabetic kidney disease.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- ITGB2 promotes HIF-1α/GLUT1 mediated glucose metabolic reprogramming in renal tubular epithelial cells to aggravate the progression of diabetic kidney disease.Cytotechnology · 2026Article
- Sodium Butyrate Attenuates Renal Fibrosis by Regulating Glycolysis and Histone H4K12 Lactylation in Diabetic Kidney Disease.Diabetes, obesity & metabolism · 2026Article
- Mrpl50 integrates glucolipotoxicity with hypoxia-inducible factor 1 alpha signaling to drive diabetic kidney disease.The Journal of biological chemistry · 2026Article
- mTORC1-signaling switches megalin function from endocytosis to cell cycle progression.Cellular and molecular life sciences : CMLS · 2026Article
- Identification of PANoptosis hub genes driving immune activation and tubulointerstitial injury in diabetic kidney disease by integrative bioinformatics and machine learning.Frontiers in immunology · 2026Article
- Lysosome stress response and mitochondria injury are the earliest detectable alteration in FSGS.Scientific reports · 2025Article
- Impact of hyperbaric oxygenation therapy (HBOT) on renal function in human.Scientific reports · 2025Article
- T cell metabolism in kidney immune homeostasis.Frontiers in immunology · 2024Review
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease. Glomerular hyperfiltration and albuminuria subject the proximal tubule (PT) to a subsequent elevation of workload, growth, and hypoxia. Hypoxia plays an ambiguous role in the development and progression of DKD and shall be clarified in our study. PT-von-Hippel-Lindau (Vhl)-deleted mouse model in combination with streptozotocin (STZ)-induced type I diabetes mellitus (DM) was phenotyped. In contrary to PT-Vhl-deleted STZ-induced type 1 DM mice, proteinuria and glomerular hyperfiltration occurred in diabetic control mice the latter due to higher nitric oxide synthase 1 and sodium and glucose transporter expression. PT Vhl deletion and DKD share common alterations in gene expression profiles, including glomerular and tubular morphology, and tubular transport and metabolism. Compared to diabetic control mice, the most significantly altered in PT Vhl-deleted STZ-induced type 1 DM mice were Ldc-1, regulating cellular oxygen consumption rate, and Zbtb16, inhibiting autophagy. Alignment of altered genes in heat maps uncovered that Vhl deletion prior to STZ-induced DM preconditioned the kidney against DKD. HIF-1α stabilization leading to histone modification and chromatin remodeling resets most genes altered upon DKD towards the control level. These data demonstrate that PT HIF-1α stabilization is a hallmark of early DKD and that targeting hypoxia prior to the onset of type 1 DM normalizes renal cell homeostasis and prevents DKD development.
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