{
  "id": 16551391,
  "title": "Cardiomyocyte Identity Crisis Without Regenerative Re-entry: A Multi-Scale Atlas of Incomplete Dedifferentiation and Intercellular Communication Rewiring in the Infarcted Human Heart",
  "url": "https://urgent.news/2026/10/25/cardiomyocyte-identity-crisis-without-regenerative-re-entry-a-multi",
  "topic": "science",
  "section": "Science",
  "published": "2026-10-25T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.10.20.760578v1?rss=1"
  },
  "original_language": "en",
  "account": "In the aftermath of a myocardial infarction, adult mammalian hearts struggle to regenerate due to a phenomenon known as incomplete dedifferentiation of cardiomyocytes. These mature heart cells largely cease participating in the cell cycle during the postnatal maturation process, but the molecular mechanisms linking maturation, disease-induced dedifferentiation, and intercellular communication remain poorly understood.\n\nTo shed light on this issue, researchers have integrated public single-cell and single-nucleus transcriptomes of developing, adult, and infarcted human and mouse hearts, alongside Visium spatial transcriptomics. This approach enabled the reconstruction of a cross-species maturation trajectory, a communication atlas detailing the role of ligand-receptor interactions, and rare-event proliferation counts utilizing donor-aware statistics.\n\nThe findings reveal that myocardial infarction triggers a partial identity loss in cardiomyocytes. This is characterized by a stress-associated switch in myosin isoforms, a collapse of the ventricular identity factor IRX4, and a decline in maturation scores. Importantly, this identity erosion occurs without any regenerative proliferative re-entry or the reactivation of fetal transcription factors. The cycling nuclei, indicative of cells in the cell cycle, remain exceedingly scarce in these infarcted heart tissues.",
  "summary": "Background: Adult mammalian hearts regenerate poorly after myocardial infarction (MI) because cardiomyocytes largely, though not absolutely, exit the cell cycle during postnatal maturation, yet the molecular logic connecting maturation, disease-associated dedifferentiation, and intercellular communication remains unclear. Methods: Public single-cell and single-nucleus transcriptomes of…",
  "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."
}