{
  "id": 12202953,
  "title": "Disease-associated mutations directionally modulate epigenetic age in iPSC-derived tissues",
  "url": "https://urgent.news/2026/10/04/disease-associated-mutations-directionally-modulate-epigenetic-age-in",
  "topic": "science",
  "section": "Science",
  "published": "2026-10-04T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.09.30.755445v1?rss=1"
  },
  "original_language": "en",
  "account": "Reprogramming somatic cells into induced pluripotent stem cells (iPSCs) has the ability to reset epigenetic age, presenting a challenge for modeling age-related cellular states and limiting the use of iPSCs in aging research beyond the genetic aspect. Research has shown that healthy organoids can re-accumulate age-related epigenetic states over long cultures; however, whether disease-associated genetic states can influence these trajectories after reprogramming remains unclear. In this study, a reproducible in-vitro method to restore epigenetic aging trajectories using iPSC-derived organoid systems is presented, as measured by various epigenetic clock models. The researchers first prove that epigenetic age steadily rises with successive passaging in a lung organoid model (alveolospheres). They then reveal that disease-associated mutations in various models induce further, intrinsic changes in epigenetic age, suggesting that disease state acts as an independent factor in modulating epigenetic clocks. These findings confirm that iPSC-derived organoids accurately mimic epigenetic aging trajectories over time, while also emphasizing disease state as a powerful and potentially easy-to-manipulate determinant of epigenetic age in a laboratory setting. This method enhances the reliability of modeling age-related cellular states, thereby expanding the applicability of iPSC-based systems in exploring the molecular mechanisms that govern human aging.",
  "summary": "Reprogramming somatic cells into induced pluripotent stem cells (iPSCs) resets epigenetic age, creating a major challenge for modeling age-associated cellular states and limiting the use of iPSCs in aging research beyond the genetic component. Recent work has shown that healthy organoids can re-accumulate age-associated epigenetic states over extended culture; whether disease-associated genetic…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}