ReviewMediators of inflammation2010
TNF superfamily: a growing saga of kidney injury modulators.
Review in Mediators of inflammation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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
52 citing papers in PubMed, 87 citations in OpenAlex.
- Trial
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- The role of ferroptosis in acute kidney injury: the preemptive mode of cell death and the bridging effect.Renal failure · 2025Review
- Senescence Biomarkers and Trajectories of Frailty and Physical Function After Kidney Transplantation.Clinical transplantation · 2024Article
- Mechanism of tacrolimus in the treatment of lupus nephritis.Frontiers in pharmacology · 2024Review
- Identification of the regulatory mechanism of ACE2 in COVID-19-induced kidney damage with systems genetics approach.Journal of molecular medicine (Berlin, Germany) · 2023Article
- N-type calcium channel and renal injury.International urology and nephrology · 2022Review
- Advances in pediatric acute kidney injury.Pediatric research · 2022Review
- Elevated Serum Osteoprotegerin is Associated with Reduced Risks of Albuminuria and CKD Progression in Patients with Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Mechanisms of Cardiorenal Protection With SGLT2 Inhibitors in Patients With T2DM Based on Network Pharmacology.Frontiers in cardiovascular medicine · 2022Article
- Development of Biomarkers and Molecular Therapy Based on Inflammatory Genes in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- Tacrolimus Prevents TWEAK-Induced PLA2R Expression in Cultured Human Podocytes.Journal of clinical medicine · 2020Article
- Dexmedetomidine Protects against Ischemia and Reperfusion-Induced Kidney Injury in Rats.Mediators of inflammation · 2020Article
- Renal tubular cell spliced X-box binding protein 1 (Xbp1s) has a unique role in sepsis-induced acute kidney injury and inflammation.Kidney international · 2019Article
- CXCL8Biological research · 2019Article
- Maresin 1 Mitigates Sepsis-Associated Acute Kidney Injury in MiceFrontiers in pharmacology · 2019Article
- Association of Soluble TNFR-1 Concentrations with Long-Term Decline in Kidney Function: The Multi-Ethnic Study of Atherosclerosis.Journal of the American Society of Nephrology : JASN · 2018Article
- Relapse of nephrotic syndrome triggered by Kawasaki disease.CEN case reports · 2018Article
- TWEAK and RIPK1 mediate a second wave of cell death during AKI.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Renal ADAM10 and 17: Their Physiological and Medical Meanings.Frontiers in cell and developmental biology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the TNF superfamily participate in kidney disease. Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. In vivo TWEAK promotes postnephrectomy compensatory renal cell proliferation in a noninflammatory milieu. However, in the inflammatory milieu of acute kidney injury, TWEAK promotes tubular cell death and inflammation. Therapeutic targeting of TNF superfamily cytokines, including multipronged approaches targeting several cytokines should be further explored.
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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 OpenQuestion graph.