ReviewCytokine & growth factor reviews2014
The TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and disease.
Review in Cytokine & growth factor reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 68 citations in OpenAlex.
- Human skeletal muscle macrophages increase following cycle training and are associated with adaptations that may facilitate growth.Scientific reports · 2019Trial
- Fn14 is an activity-dependent, Bmal1-regulated cytokine receptor that induces rod-like microglia and restricts neuronal activity in vivo.Cell reports · 2026Article
- A single day of reduced activity alters the next day's transcriptomic and metabolic exercise response.American journal of physiology. Endocrinology and metabolism · 2026Article
- Inhibition of TWEAK/Fn14 Ameliorates Sarcopenic Obesity by Restoring Mitochondrial Biogenesis via the AMPK/SIRT1/PGC-1α Axis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Investigating the Role of TNFSF12 in Thyroid Cancer Progression via Single-Cell RNA Sequencing and Integrated Multiomics Analyses.Mediators of inflammation · 2026Article
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Article
- Sarcopenia: Current Insights into Molecular Mechanisms, Diagnostics, and Emerging Interventional Approaches.International journal of molecular sciences · 2025Review
- Patients Having Major Abdominal Cancer Surgery Exhibit Significant Acute Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.JCI insight · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.bioRxiv : the preprint server for biology · 2025Article
- Article
- Chronic circadian misalignment accelerates sarcopenia progression in mice.Frontiers in physiology · 2025Article
- The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia.Cancer cell · 2024Article
- Exercise microdosing for skeletal muscle health applications to spaceflight.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- The cytokine receptor Fn14 is a molecular brake on neuronal activity that mediates circadian functionbioRxiv : the preprint server for biology · 2024Article
- Fn14 promotes myoblast fusion during regenerative myogenesis.Life science alliance · 2023Article
- Article
- Multitissue responses to exercise: a MoTrPAC feasibility study.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
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
TNF-like weak inducer of apoptosis (TWEAK), a TNF superfamily ligand, and its bona fide receptor, the TNF receptor superfamily member fibroblast growth factor-inducible 14 (Fn14), represent a pivotal axis for shaping both physiological and pathological tissue responses to acute or chronic injury and disease. In recent years significant advances have been made in delineating the prominent role of TWEAK-Fn14 dyad in regulating skeletal muscle mass and metabolism. Also emerging from the broad study of tissue injury in skeletal muscle and other organs is the role of the TWEAK-Fn14 pathway in promoting fibrosis. This review article highlights recent advancements toward understanding how the TWEAK-Fn14 pathway regulates the response to various skeletal muscle insults and, more broadly, engages multiple mechanisms to drive tissue fibrosis.
Indexed as
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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.