ReviewAdvances in chronic kidney disease2014
Podocytes, signaling pathways, and vascular factors in diabetic kidney disease.
Review in Advances in chronic kidney disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Deciphering the Role of Sirtuin-1 Gene Polymorphism in Diabetic Nephropathy: A Systematic Review and Meta-Analysis.Journal of diabetes research · 2026Pooled it
- The effect of SGLT2 inhibitor and HIF-PHI on the podocyte-specific molecules and cytoskeleton of diabetic podocytes.BMC nephrology · 2025Article
- Renal microcirculation and mechanisms in diabetic kidney disease.Frontiers in endocrinology · 2025Review
- Cyclin-dependent kinase 5 as a potential therapeutic target to alleviate high glucose-induced podocyte apoptosis and hyperglycemia-induced renal injury in mice.Histology and histopathology · 2025Article
- Article
- Lipid metabolism disorder in diabetic kidney disease.Frontiers in endocrinology · 2024Review
- Characterization of immortalized human podocytes infected with lentivirus as anAmerican journal of clinical and experimental immunology · 2024Article
- The therapeutic prospect of zinc oxide nanoparticles in experimentally induced diabetic nephropathy.Tissue barriers · 2023Article
- Fisetin Ameliorates Diabetic Nephropathy-Induced Podocyte Injury by Modulating Nrf2/HO-1/GPX4 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Subclinical signs of podocyte injury associated with Circulating Anodic Antigen (CAA) in Schistosoma mansoni-infected patients in Brazil.Revista da Sociedade Brasileira de Medicina Tropical · 2023Article
- The role of protein kinase C in diabetic microvascular complications.Frontiers in endocrinology · 2022Review
- miR-188-3p abolishes germacrone-mediated podocyte protection in a mouse model of diabetic nephropathy in type I diabetes through triggering mitochondrial injury.Bioengineered · 2022Article
- The expression of apoptosis related genes in HK-2 cells overexpressingFrontiers in genetics · 2022Article
- Long non-cording RNA XIST promoted cell proliferation and suppressed apoptosis by miR-423-5p/HMGA2 axis in diabetic nephropathy.Molecular and cellular biochemistry · 2021Article
- Injection of hybrid 3D spheroids composed of podocytes, mesenchymal stem cells, and vascular endothelial cells into the renal cortex improves kidney function and replenishes glomerular podocytes.Bioengineering & translational medicine · 2021Article
- Screening and Analysis of Key Genes in miRNA-mRNA Regulatory Network of Membranous Nephropathy.Journal of healthcare engineering · 2021Article
- Molecular Mechanisms in Early Diabetic Kidney Disease: Glomerular Endothelial Cell Dysfunction.International journal of molecular sciences · 2020Review
- Modulation of proteomic and inflammatory signals by Bradykinin in podocytes.Journal of advanced research · 2020Article
- MicroRNA-145-5p attenuates high glucose-induced apoptosis by targeting the Notch signaling pathway in podocytes.Experimental and therapeutic medicine · 2020Article
- Morroniside Inhibits HFrontiers in pharmacology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Alterations and injury to glomerular podocytes play a key role in the initiation and progression of diabetic kidney disease (DKD). Multiple factors in diabetes cause abnormalities in podocyte signaling that lead to podocyte foot process effacement, hypertrophy, detachment, loss, and death. Alterations in insulin action and mammalian target of rapamycin activation have been well documented to lead to pathology. Reduced insulin action directly leads to albuminuria, increased glomerular matrix accumulation, thickening of the glomerular basement membrane, podocyte apoptosis, and glomerulosclerosis. In addition, podocytes generate factors that alter signaling in other glomerular cells. Prominent among these is vascular endothelial growth factor-A, which maintains glomerular endothelium viability but causes endothelial cell pathology when generated at too high a level. Finally, circulating vascular factors (eg, activated protein C) have a profound effect on podocyte stability and survival. This cytoprotective factor is critical for podocyte health, and its deficiency promotes podocyte injury and apoptosis. Thus, the podocyte sits in the center of a network of paracrine and hormonal signaling systems that in health keep the podocyte adaptable and viable, but in diabetes they can lead to pathologic changes, detachment, and death.
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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 Socratic graph.