ArticleAmerican journal of physiology. Renal physiology2016
Podocyte injury: the role of proteinuria, urinary plasminogen, and oxidative stress.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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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Who cites it
34 citing papers in PubMed, 68 citations in OpenAlex.
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Nicotinamide mononucleotide protects against diabetic nephropathyWorld journal of diabetes · 2025Article
- Notch signaling in diabetic kidney disease: recent progress.Frontiers in endocrinology · 2025Review
- Genetically conditioned interaction among microRNA-155, alpha-klotho, and intra-renal RAS in male rats: Link to CKD progression.Physiological reports · 2024Article
- Urinary Plasminogen as a Marker of Disease Progression in Human Glomerular Disease.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024Article
- Serum cell division cycle 42 reflects the development and progression of diabetic nephropathy in patients with diabetes mellitus.Experimental and therapeutic medicine · 2024Article
- A Serine Protease Inhibitor, Camostat Mesilate, Suppresses Urinary Plasmin Activity and Alleviates Hypertension and Podocyte Injury in Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- Article
- Renal and Inflammatory Proteins as Biomarkers of Diabetic Kidney Disease and Lupus Nephritis.Oxidative medicine and cellular longevity · 2022Article
- Sulfuretted hydrogen ameliorates high dose glucose-induced podocyte apoptosis via orchestrating AMPK/mTOR cascade-mediated anti-apoptotic effects.Annals of translational medicine · 2021Article
- PP2A protects podocytes against Adriamycin-induced injury and epithelial-to-mesenchymal transition via suppressing JIP4/p38-MAPK pathway.Cytotechnology · 2021Article
- Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice.Disease models & mechanisms · 2021Article
- Shensu IV prevents glomerular podocyte injury in nephrotic rats via promoting lncRNA H19/DIRAS3-mediated autophagy.Bioscience reports · 2021Article
- Nicotine, smoking, podocytes, and diabetic nephropathy.American journal of physiology. Renal physiology · 2021Article
- Mitochondrial Disease and the Kidney With a Special Focus on CoQKidney international reports · 2020Review
- Plasminogenuria is associated with podocyte injury, edema, and kidney dysfunction in incident glomerular disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Plasminogen Deficiency and Amiloride Mitigate Angiotensin II-Induced Hypertension in Type 1 Diabetic Mice Suggesting Effects Through the Epithelial Sodium Channel.Journal of the American Heart Association · 2020Article
- Pyrroloquinoline Quinone Inhibits Oxidative Stress in Rats with Diabetic Nephropathy.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Oxidative Storm Induced by Tryptophan Metabolites: Missing Link between Atherosclerosis and Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Podocytes are the key target for injury in proteinuric glomerular diseases that result in podocyte loss, progressive focal segmental glomerular sclerosis (FSGS), and renal failure. Current evidence suggests that the initiation of podocyte injury and associated proteinuria can be separated from factors that drive and maintain these pathogenic processes leading to FSGS. In nephrotic urine aberrant glomerular filtration of plasminogen (Plg) is activated to the biologically active serine protease plasmin by urokinase-type plasminogen activator (uPA). In vivo inhibition of uPA mitigates Plg activation and development of FSGS in several proteinuric models of renal disease including 5/6 nephrectomy. Here, we show that Plg is markedly increased in the urine in two murine models of proteinuric kidney disease associated with podocyte injury: Tg26 HIV-associated nephropathy and the Cd2ap
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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.