ReviewReviews in endocrine & metabolic disorders2022
The TWEAK/Fn14/CD163 axis-implications for metabolic disease.
Review in Reviews in endocrine & metabolic disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05347836 (Monocyte Soluble Activation Markers sCD14 and sCD163 in Children With Type 1 Diabetes Mellitus), which is not on this map. Cited by 43 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.
Monocyte Soluble Activation Markers sCD14 and sCD163 in Children With Type 1 Diabetes Mellitus
Who cites it
43 citing papers in PubMed, 67 citations in OpenAlex.
- Ethanolamine as a potential biomarker and therapeutic target for depressive disorder.Molecular psychiatry · 2026Article
- A Transcriptomic Analysis of Cancer-Stromal Interactome in Lung Cancer Xenograft Models.Cancer science · 2026Article
- Serum sCD163 indicates disease severity and prognosis in sudden sensorineural hearing loss.Molecular medicine (Cambridge, Mass.) · 2026Article
- Iparomlimab and tuvonralimab (QL1706) combined definitive chemoradiotherapy in patients with locally advanced esophageal squamous cell carcinoma (QL1706-IIT-02): a single arm, phase 2 trial.EClinicalMedicine · 2026Article
- In Vitro Analysis of TWEAK/Fn14 Axis in the Blood-Brain Barrier Models during Oxygen-Glucose Deprivation and Reoxygenation.Molecular neurobiology · 2026Article
- Association of programmed cell death with atrial fibrillation risk: A multi-omics Mendelian randomization study.Medicine · 2026Article
- TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF‑κB pathway.International journal of molecular medicine · 2026Article
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Integrating multi-omics, EWAS, and reverse network toxicology to explore environmental pollutant risks in erectile dysfunction.Frontiers in cell and developmental biology · 2026Article
- Strength in numbers: how multimerization drives HpHb uptake by CD163 scavenging receptor.Nature communications · 2025Article
- Expression and significance ofBiomarkers in medicine · 2025Article
- Identification of circulating inflammation cytokines as a mediator of gut microbiota and type 2 diabetes mellitus: a Mendelian randomization study.Diabetology & metabolic syndrome · 2025Article
- Distinct Alterations of Inflammatory Biomarkers in Cluster Headache: A Case Control Study.Annals of neurology · 2025Article
- Structural elucidation of the haptoglobin-hemoglobin clearance mechanism by macrophage scavenger receptor CD163.PLoS biology · 2025Article
- Synergistic effects of LCN2 and TWEAK on the progression of psoriasis.Cellular & molecular immunology · 2025Article
- Baicalin Alleviates Piglet Immunosuppression Induced byBiomolecules · 2025Article
- Review
- Dynamic single cell transcriptomics defines kidney FGF23/KL bioactivity and novel segment-specific inflammatory targets.Kidney international · 2025Article
- Molecular differences between young and mature stria vascularis from organotypic explants and transcriptomics.iScience · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TWEAK (tumor necrosis factor-like weak inducer of apoptosis) is a member of the TNF superfamily that controls a multitude of cellular events including proliferation, migration, differentiation, apoptosis, angiogenesis, and inflammation. TWEAK control of these events is via an expanding list of intracellular signalling pathways which include NF-κB, ERK/MAPK, Notch, EGFR and AP-1. Two receptors have been identified for TWEAK - Fn14, which targets the membrane bound form of TWEAK, and CD163, which scavenges the soluble form of TWEAK. TWEAK appears to elicit specific events based on the receptor to which it binds, tissue type in which it is expressed, specific extrinsic conditions, and the presence of other cytokines. TWEAK signalling is protective in healthy tissues, but in chronic inflammatory states become detrimental to the tissue. Consistent data show a role for the TWEAK/FN14/CD163 axis in metabolic disease, chronic autoimmune diseases, and acute ischaemic stroke. Low circulating concentrations of soluble TWEAK are predictive of poor cardiovascular outcomes in those with and without diabetes. This review details the current understanding of the TWEAK/Fn14/CD163 axis as one of the chief regulators of immune signalling and its cell-specific role in metabolic disease development and progression.
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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.