ReviewNephron extra
Effects of Tumor Necrosis Factor-α on Podocyte Expression of Monocyte Chemoattractant Protein-1 and in Diabetic Nephropathy.
Review in Nephron extra. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Biomarkers to predict or measure steroid resistance in idiopathic nephrotic syndrome: A systematic review.PloS one · 2025Pooled it
- Titanium Dioxide Exacerbates Calcium Phosphate and Urate-Induced Oxidative Stress, Injury and Inflammatory Response in Human Kidney-2 Cells.Journal of biochemical and molecular toxicology · 2026Article
- Tubular Epithelia-Specific Deletion of MCP-1 Does Not Afford Protection Against Adriamycin-Induced Kidney Injury.International journal of molecular sciences · 2026Article
- Hyperglycaemia-induced molecular reprogramming of proximal tubular epithelial cells and its contribution to diabetic kidney disease progression-a narrative review.Frontiers in cell and developmental biology · 2026Review
- REDD1 expression in podocytes facilitates renal inflammation and pyroptosis in streptozotocin-induced diabetic nephropathy.Cell death & disease · 2025Article
- Surrogate endpoints in diabetic kidney disease: current perspectives and future directions.Frontiers in endocrinology · 2025Review
- A human stem cell-derived model reveals pathologic extracellular matrix remodeling in diabetic podocyte injury.Matrix biology plus · 2024Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Podocyte-Specific Deletion of MCP-1 Fails to Protect against Angiotensin II- or Adriamycin-Induced Glomerular Disease.International journal of molecular sciences · 2024Article
- Mesenchymal stem cells enhance CCL8 expression by podocytes in lupus-prone MRL.FasScientific reports · 2023Article
- The use of plasma biomarker-derived clusters for clinicopathologic phenotyping: results from the Boston Kidney Biopsy Cohort.Clinical kidney journal · 2023Article
- Glucosidase inhibitor, Nimbidiol ameliorates renal fibrosis and dysfunction in type-1 diabetes.Scientific reports · 2022Article
- Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.The Journal of experimental medicine · 2022Article
- Sevoflurane preconditioning prevents acute renal injury caused by ischemia-reperfusion in mice via activation of the Nrf2 signaling pathway.Experimental and therapeutic medicine · 2022Article
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- LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition.Journal of cellular biochemistry · 2020Article
- Autoimmunity in Focal Segmental Glomerulosclerosis: A Long-Standing Yet Elusive Association.Frontiers in medicine · 2020Review
- Podocytes contribute, and respond, to the inflammatory environment in lupus nephritis.American journal of physiology. Renal physiology · 2018Article
- Rice bran protein hydrolysates attenuate diabetic nephropathy in diabetic animal model.European journal of nutrition · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
BACKGROUND/
aimsTumor necrosis factor (TNF)-α is believed to play a role in diabetic kidney disease. This study explores the specific effects of TNF-α with regard to nephropathy-relevant parameters in the podocyte.
methodsCultured mouse podocytes were treated with recombinant TNF-α and assayed for production of monocyte chemoattractant protein-1 (MCP-1) by enzyme-linked immunosorbent assay (ELISA). TNF-α signaling of MCP-1 was elucidated by antibodies against TNF receptor (TNFR) 1 or TNFR2 or inhibitors of nuclear factor-kappaB (NF-κB), phosphatidylinositol 3-kinase (PI3K) or Akt. In vivo studies were done on male db/m and type 2 diabetic db/db mice. Levels of TNF-α and MCP-1 were measured by RT-qPCR and ELISA in the urine, kidney and plasma of the two cohorts and correlated with albuminuria.
resultsPodocytes treated with TNF-α showed a robust increase (∼900%) in the secretion of MCP-1, induced in a dose- and time-dependent manner. Signaling of MCP-1 expression occurred through TNFR2, which was inducible by TNF-α ligand, but did not depend on TNFR1. TNF-α then proceeded via the NF-κB and the PI3K/Akt systems, based on the effectiveness of the inhibitors of those pathways. For in vivo relevance to diabetic kidney disease, TNF-α and MCP-1 levels were found to be elevated in the urine of db/db mice but not in the plasma.
conclusionTNF-α potently stimulates podocytes to produce MCP-1, utilizing the TNFR2 receptor and the NF-κB and PI3K/Akt pathways. Both TNF-α and MCP-1 levels were increased in the urine of diabetic db/db mice, correlating with the severity of diabetic albuminuria.
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What OpenQuestion holds
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.