ReviewInternational journal of molecular sciences2022
The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Upregulated Klotho expression reflects a potential compensatory renal response in Trimethyltin-exposed rats.Medical molecular morphology · 2026Article
- Network Pharmacology Combined With Metabonomics and Transcriptomics Reveals the Mechanism ofFood science & nutrition · 2026Article
- Unveiling the therapeutic potential of gut microbiota metabolites for the treatment of renal fibrosis based on network pharmacology study.Bioresources and bioprocessing · 2026Article
- Systemic inflammatory profiles are associated with long-term kidney failure and patient mortality in chronic kidney disease.Clinical kidney journal · 2026Article
- Dysregulated Bone Marrow Contributes to Glomerular Injury through Soluble Factors.Journal of the American Society of Nephrology : JASN · 2026Article
- Moringa Peregrina-derived Selenium Nanoparticles: Potent Inhibitor of Key Inflammatory Pathways in Aluminum-exposed Rats.Pharmaceutical nanotechnology · 2026Article
- Exploring the protective role of DDIT4/mTOR in podocyte integrity through macrophage polarization in diabetic kidney disease.Renal failure · 2025Article
- Association of MASLD with Baseline and New-Onset Liver Function Test Elevation in Medical ICU Patients.Medicina (Kaunas, Lithuania) · 2025Article
- Article
- From Liver to Kidney: The Overlooked Burden of Nonalcoholic Fatty Liver Disease in Chronic Kidney Disease.Journal of clinical medicine · 2025Review
- Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators.International journal of molecular sciences · 2025Review
- Treatment outcomes and determinants of combined hemodialysis-hemoperfusion therapy in chronic glomerulonephritis.American journal of translational research · 2025Article
- Ethnicity-specific associations between the promoter region G-308A polymorphism (rs1800629) of the TNF-α gene and the development of end-stage renal disease: An evidence-based meta-analysis and trial sequential analysis.Genetics and molecular biology · 2025Article
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Chronic Kidney Disease-associated Lung Injury Is Mediated by Phosphate-induced MAPK/AKT Signaling.American journal of respiratory cell and molecular biology · 2024Article
- Role of baseline soluble tumor necrosis factor receptor 2 as a biomarker in primary podocytopathy: Implications for renal impairment and disease progression.BMC nephrology · 2024Article
- Nuclear receptor 4A1 ameliorates UUO-induced renal fibrosis by inhibiting the PI3K/AKT pathway.Scientific reports · 2024Article
- TMAO enhances TNF-α mediated fibrosis and release of inflammatory mediators from renal fibroblasts.Scientific reports · 2024Article
- Interleukin-10 enhances recruitment of immune cells in the neonatal mouse model of obstructive nephropathy.Scientific reports · 2024Article
- Natural Polyphenols in Cancer Management: Promising Role, Mechanisms, and Chemistry.Current pharmaceutical biotechnology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic kidney disease (CKD) has been recognized as a global public health problem. Despite the current advances in medicine, CKD-associated morbidity and mortality remain unacceptably high. Several studies have highlighted the contribution of inflammation and inflammatory mediators to the development and/or progression of CKD, such as tumor necrosis factor (TNF)-related biomarkers. The inflammation pathway driven by TNF-α, through TNF receptors 1 (TNFR1) and 2 (TNFR2), involves important mediators in the pathogenesis of CKD. Circulating levels of TNFRs were associated with changes in other biomarkers of kidney function and injury, and were described as predictors of disease progression, cardiovascular morbidity, and mortality in several cohorts of patients. Experimental studies describe the possible downstream signaling pathways induced upon TNFR activation and the resulting biological responses. This review will focus on the available data on TNFR1 and TNFR2, and illustrates their contributions to the pathophysiology of kidney diseases, their cellular and molecular roles, as well as their potential as CKD biomarkers. The emerging evidence shows that TNF receptors could act as biomarkers of renal damage and as mediators of the disease. Furthermore, it has been suggested that these biomarkers could significantly improve the discrimination of clinical CKD prognostic models.
Indexed as
Identifiers
What Socratic 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 Socratic graph.