ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
Glomerular VEGF resistance induced by PKCδ/SHP-1 activation and contribution to diabetic nephropathy.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- A systematic review of urinary extracellular vesicle-derived non-coding RNAs in diabetic nephropathy: expression profiles, clinical correlations, and diagnostic performance.Molecular biology reports · 2026Pooled it
- Research trends and frontiers of the Apelin system in kidney diseases: a multi-database bibliometric analysis and cross-validation study.International urology and nephrology · 2026Review
- Advances in targeted treatment of ferroptosis in diabetic kidney disease with SGLT2 inhibitors.Diabetology & metabolic syndrome · 2026Review
- A case of lupus nephritis achieving early remission using a treatment protocol similar to the AURORA trial with voclosporin and successfully discontinuing corticosteroids early.CEN case reports · 2026Article
- Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation.Journal of advanced research · 2026Article
- Study on the Potential Mechanism of Bisphenol A-induced Human Diabetic Nephropathy Based on Network Toxicology and Molecular Docking.Endocrine, metabolic & immune disorders drug targets · 2026Article
- The effect of SGLT2 inhibitor and HIF-PHI on the podocyte-specific molecules and cytoskeleton of diabetic podocytes.BMC nephrology · 2025Article
- Effect of dapagliflozin on eGFR slope in IgA nephropathy based on renal pathological assessment using image analysis software.Metabolism open · 2025Article
- Intravitreal vascular endothelial growth factor inhibitor systemic and renal toxicity registry.Clinical kidney journal · 2025Article
- Article
- Recent advances in understanding the mechanisms by which sodium-glucose co-transporter type 2 inhibitors protect podocytes in diabetic nephropathy.Diabetology & metabolic syndrome · 2025Article
- New Insights into the Pleiotropic Actions of Dipeptidyl Peptidase-4 Inhibitors Beyond Glycaemic Control.TouchREVIEWS in endocrinology · 2024Review
- Article
- Inhibition of PKC-δ retards kidney fibrosis via inhibiting cGAS-STING signaling pathway in mice.Cell death discovery · 2024Article
- Upregulation of rate-limiting enzymes in cholesterol metabolism by PKCδ mediates endothelial apoptosis in diabetic wound healing.Cell death discovery · 2024Article
- Protective Factors and the Pathogenesis of Complications in Diabetes.Endocrine reviews · 2024Review
- Article
- Role and Mechanism of Growth Differentiation Factor 15 in Chronic Kidney Disease.Journal of inflammation research · 2024Review
- Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023Review
- PKCδ regulates the vascular biology in diabetic atherosclerosis.Cell communication and signaling : CCS · 2023Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
This study characterizes the effect of glucose-induced activation of protein kinase Cδ (PKCδ) and Src homology-2 domain-containing phosphatase-1 (SHP-1) expression on vascular endothelial growth factor (VEGF) actions in glomerular podocytes in cultures and in glomeruli of diabetic rodents. Elevation of glucose levels induced PKCδ and p38 mitogen-activated protein kinase (p38 MAPK) to increase SHP-1 expression, increased podocyte apoptosis, and inhibited VEGF activation in podocytes and glomerular endothelial cells. The adverse effects of high glucose levels can be negated by molecular inhibitors of PKCδ, p38MAPK, and SHP-1 and only partially reduced by antioxidants and nuclear factor-κB (NF-κB) inhibitor. Increased PKCδ activation and SHP-1 expression correlated with loss of VEGF signaling and podocyte numbers in the glomeruli of diabetic rats and mice. In contrast, diabetic PKCδ-knockout (Prkcd(-/-)) mice did not exhibit activation of p38 MAPK and SHP-1 or inhibition of VEGF signaling in renal glomeruli. Functionally, diabetic Prkcd(-/-) mice had decreased expressions of TGFβ, VEGF, and extracellular matrix and less albuminuria than diabetic Prkcd(+/+) mice. Hyperglycemia and diabetes can cause glomerular podocyte apoptosis and endothelial dysfunction partly due to increased PKCδ/p38 MAPK activation and the expression of SHP-1 to cause VEGF resistance, independent of NF-κB activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.