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Neural mechanisms underlying strain preference behaviour and plasticity in mice
Creation of a eukaryotic multiplexed site-specific inversion system and its application for metabolic engineering
Memorability of novel words correlates with anterior fusiform activity during reading
Preclinical tumor control with a laser-accelerated high-energy electron radiotherapy prototype
A tunable entangled photon-pair source based on a Van der Waals insulator
Droplet-supported liquid-liquid lateral phase separation as a step to floating protein heterostructures
Dual-mode action of scalable, high-quality engineered stem cell-derived SIRPα-extracellular vesicles for treating acute liver failure
A concise enzyme cascade enables the manufacture of natural and halogenated protoberberine alkaloids
Pluripotency factor Tex10 finetunes Wnt signaling for spermatogenesis and primordial germ cell development
Electrochemical epoxidation enhanced by C2H4 activation and hydroxyl generation at the Ag/SnO2 interface
Redox profiling of preovulatory follicular fluid in the donkey is species-specific, and contributes to modulate sperm function
Coupling of electronic transition to ferroelectric order in a 2D semiconductor
Vascular access dysfunction incidence among Japanese dialysis patients from NDB Open Data Japan
Increased ectodysplasin-A2-receptor EDA2R is a ubiquitous hallmark of aging and mediates parainflammatory responses
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.