ArticleNature communications2025
Increased ectodysplasin-A2-receptor EDA2R is a ubiquitous hallmark of aging and mediates parainflammatory responses.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Longitudinal Dynamics of the Blood Proteome Within the Alzheimer Spectrum in Down Syndrome.Neurology · 2026Article
- Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice.Nature communications · 2026Article
- Longitudinal plasma proteomics separates diagnostic differences from progression-linked changes in Alzheimer's disease.medRxiv : the preprint server for health sciences · 2026Article
- A personalized genomic-medicine approach to rare genomic disorders associated with simple chromosomal structural variants.HGG advances · 2026Article
- Plasma proteomic signatures predict incident benign prostatic hyperplasia: a prospective cohort study of 20 996 men.Journal of global health · 2026Article
- Article
- Proteomic aging clocks in epidemiological studies: advances, applications and prospects.Nature aging · 2026Review
- Multiblock proteomic profiling identifies novel biomarkers linking prediabetes with preclinical atherosclerosis in apparently healthy adults.Cardiovascular diabetology · 2026Article
- Reduced osteogenic factors and early osteoblast senescence in SOD1(G93A) ALS mouse model.JCI insight · 2026Article
- ORANGE: a machine learning approach for modeling tissue-specific aging from transcriptomic data.Briefings in bioinformatics · 2026Article
- Age effect explorer: a Shiny application to browse and visualize tissue-specific age-related gene expression changes.Bioinformatics advances · 2026Article
- CSF estrogens' relationships to neuroinflammatory markers and brain networks in middle-aged and older black and white women.Journal of neuroinflammation · 2025Article
- Impact of Exercise Modalities on Pentraxin-3 (PTX3) Levels: A Systematic Review and Meta-Analysis.Muscles (Basel, Switzerland) · 2025Review
- Proteomic signature of metabolic dysfunction-associated steatotic liver disease and risk of atherosclerotic cardiovascular disease.Cardiovascular diabetology · 2025Article
- The Roles of EDA2R in Ageing and Disease.Aging cell · 2025Review
- Targeting PURPL RNA enabled rejuvenation of senescence cells via epigenetic reprogramming.Journal of translational medicine · 2025Article
- A multi-omics investigation of sarcopenia and frailty: Integrating genomic, epigenomic and telomere length data.Experimental physiology · 2025Article
- Using RNA therapeutics to promote healthy aging.Nature aging · 2025Review
- Plasma Proteomics Reveals Biomarkers and Undulating Changes in Metabolic Aging.Research (Washington, D.C.) · 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
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intensive efforts have been made to identify features that could serve as biomarkers of aging. Yet, drug-based interventions aimed at lessening the detrimental effects of getting older are lacking. This is largely attributable to tissue-specificity, sex-related differences, and to the difficulty of identifying actionable targets, which continues to pose a significant challenge. Here, we implement a bioinformatics approach revealing that aging-associated increase of the transmembrane Ectodysplasin-A2-Receptor is a prominent tissue-independent alteration occurring in humans and other species, and is particularly pronounced in models of accelerated aging. We show that strengthening of the Ectodysplasin-A2-Receptor signalling axis in myogenic precursors and differentiated myotubes suffices to trigger potent parainflammatory responses, mirroring aspects of aging-driven sarcopenia. Intriguingly, obesity, insulin-resistance, and aging-related comorbidities, such as type-2-diabetes, result in heightened levels of the Ectodysplasin-A2 ligand. Our findings suggest that targeting the Ectodysplasin-A2 surface receptor represents a promising pharmacological strategy to mitigate the development of aging-associated phenotypes.
Indexed as
Identifiers
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.