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<p>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.</p>

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Increased ectodysplasin-A2-receptor EDA2R is a ubiquitous hallmark of aging and mediates parainflammatory responses

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月23日

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  • Maria Chiara Barbera,
  • Luca Guarrera,
  • Andrea David Re Cecconi,
  • Giada Andrea Cassanmagnago,
  • Arianna Vallerga,
  • Martina Lunardi,
  • Francesca Checchi,
  • Laura Di Rito,
  • Margherita Romeo,
  • Sarah Natalia Mapelli,
  • Benedikt Schoser,
  • Edward V. Generozov,
  • Rinat I. Sultanov,
  • Alexandra Kanygina,
  • Nikolay A. Kulemin,
  • Ekaterina A. Semenova,
  • Rick Jansen,
  • Eco J. C. de Geus,
  • Brenda Penninx,
  • Jenny van Dongen,
  • Ilaria Craparotta,
  • Rosanna Piccirillo,
  • Ildus I. Ahmetov,
  • Marco Bolis

摘要

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.