ArticleRenal failure2022
TNF-α-mediated podocyte injury via the apoptotic death receptor pathway in a mouse model of IgA nephropathy.
Article in Renal failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease.Cell death discovery · 2026Article
- Dynamics of chromatin accessibility governing Gd-IgA1 synthesis in B cells associated with IgA nephropathy.Experimental & molecular medicine · 2025Article
- Protective effects of Staphylococcal Enterotoxin B (SEB) toxoid on lung and liver tissue integrity in rats during systemic infection.Iranian journal of microbiology · 2025Article
- Network Pharmacological Analysis of Hydroxychloroquine Intervention in the Treatment of Iga Nephropathy.Current pharmaceutical design · 2025Article
- Urinary exosomal miR-320b as a biomarker of tubular atrophy/interstitial fibrosis in IgA nephropathy patients.American journal of translational research · 2025Article
- Mechanistic insights into Shenqi Dihuang decoction in the treatment of immunoglobulin a nephropathy.Frontiers in pharmacology · 2025Article
- The Role of Macrophage Death in Periodontitis: A Review.Inflammation · 2024Review
- The Role of TNF-α in the Pathogenesis of Idiopathic Nephrotic Syndrome and Its Usefulness as a Marker of the Disease Course.Journal of clinical medicine · 2024Article
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIgA nephropathy (IgAN) is the most common primary glomerular disease worldwide and it is characterized by mesangial IgA deposits. Proteinuria is a common clinical feature of IgAN, which has a critical connection to podocyte injury and has been used as a clinical prognostic factor for IgAN. Evidence has shown that TNF-α released from mesangial cells may lead to podocyte apoptosis.
methodsForty male BALB/c mouse were randomly divided into the control group and IgAN group. A mice model of IgAN was developed by oral administration of bovine serum albumin (BSA) combined with Staphylococcus Enterotoxin B (SEB) tail vein injection. Urinary protein concentrations, renal function, renal morphological, IgA deposition, apoptosis situation, and the mRNA and protein expression of nephrin, podocin, TNF-α, TNFR1, caspase-8 and caspase-3, were detected after 12 weeks.
resultsBSA and SEB can successfully establish an IgAN mouse model, and the main pathological changes are the IgA immune complex deposition in the mesangial area. The gene and protein expression levels of nephrin and podocin were found to be downregulated, and death receptor pathway-related indicators were upregulated, and they were involved in TNF-α-activated podocyte injury and apoptosis in IgAN mice.
conclusionTNF-α may play an important role in the pathogenesis of podocyte apoptosis in IgAN, and its effects may be mediated through the apoptotic death receptor pathway.
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