{
  "abstract": "Cellular senescence has emerged as a key contributor to age-related skeletal deterioration; however, the defining characteristics of senescent osteoblasts remain incompletely understood, hindering efforts to identify the cellular mechanisms that drive age-associated bone loss and potential therapeutic targets. Here, we compared doxorubicin- and hydrogen peroxide-induced senescence and established a robust in vitro osteoblast model that enables the stable maintenance of stress-induced premature senescence. Doxorubicin-treated MC3T3-E1 cells exhibited persistent growth arrest, a pronounced senescence-associated secretory phenotype (SASP), and impaired osteogenic function accompanied by marked mitochondrial dysfunction, including reduced respiratory capacity and altered mitochondrial morphology. Transcriptomic comparison with aged murine bone revealed a partial overlap with in vivo aging-associated gene expression signatures, particularly among genes involved in extracellular matrix organization and skeletal development, supporting the physiological relevance of the model. Importantly, key features of senescence, including the senescence-associated mitochondrial phenotype and impaired osteogenic capacity, were recapitulated in primary human osteoblasts. Collectively, these findings establish a robust model of stress-induced osteoblast senescence and demonstrate that senescent osteoblasts exhibit mitochondrial dysfunction, impaired osteogenic capacity, and molecular features that resemble aspects of skeletal aging.",
  "abstract_shown": true,
  "affiliations": [
    "University Ulm"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 10,
  "authors": [
    {
      "name": "T. Frey"
    },
    {
      "name": "H. Vogg"
    },
    {
      "name": "M. Ahmad"
    },
    {
      "name": "Y. Nakano"
    },
    {
      "name": "M. Vogel"
    },
    {
      "name": "S. Nungess"
    },
    {
      "name": "A. Schoppa"
    },
    {
      "name": "H. Geiger"
    },
    {
      "name": "A. Ignatius"
    },
    {
      "affs": [
        0
      ],
      "name": "J. Riegger"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/8bjqzks32yvaz.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.09.13.751251",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.13.751251v1.full",
  "id": "8bjqzks32yvaz",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.09.13.751251v1",
  "language": null,
  "licence": "CC-BY-NC",
  "licence_label": "CC BY-NC",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "cell biology"
    ],
    [
      "openalex",
      "2737|Telomeres, Telomerase, and Senescence"
    ]
  ],
  "openalex": "W7213445630",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.13.751251v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-13",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/8bjqzks32yvaz.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:22:51Z",
      "native_id": "10.64898/2026.09.13.751251",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.13.751251v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:cell biology",
      "subfield": "cell-biology"
    }
  ],
  "title": "Mitochondrial dysfunction and impaired osteogenic capacity define stress-induced osteoblast senescence",
  "title_text": "Mitochondrial dysfunction and impaired osteogenic capacity define stress-induced osteoblast senescence",
  "type": "preprint",
  "updated_at": "2026-10-30T12:22:51Z",
  "url": "https://research.draconitic.com/paper/8bjqzks32yvaz",
  "venue": "bioRxiv",
  "versions": []
}