{
  "abstract": "Background: Silicosis is a progressive, irreversible fibrotic lung disease caused by long‐term exposure to crystalline silica. Although the anti‐fibrotic tetrapeptide Ac‐SDKP has shown promise in reducing fibrosis, the specific molecular mechanisms through which it modulates apoptosis in silica‐induced lung injury remain unclear, particularly the role of heat shock protein 27 (HSP27).\n\nMethods: Wistar rats were divided into groups including control, model (2‐week, 3‐week, and 4‐week), and Ac‐SDKP prevention/treatment groups. In vitro, MEF and A549 cells were treated with TGF‐β1 and Ac‐SDKP to observe the effects on apoptosis‐related proteins. Additionally, HSP27 interference vectors were constructed to study its role in regulating apoptosis via FAS/FASL and mitochondrial pathways in both in vivo and in vitro models.\n\nResults: In vivo, Ac‐SDKP administration alleviated silica‐induced pulmonary fibrosis and reduced apoptosis in lung tissue. In contrast, in vitro, TGF‐β1 stimulation suppressed apoptosis in A549 and MEF cells, whereas Ac‐SDKP restored apoptotic activity by regulating the HSP27‐mediated FAS/FASL and mitochondrial pathways. Moreover, AAV9‐mediated knockdown of HSP27 in mice enhanced apoptosis and attenuated fibrosis, confirming the anti‐apoptotic role of HSP27 in silicosis.\n\nConclusion: These findings reveal that Ac‐SDKP exerts context‐dependent modulation of apoptosis through HSP27—protecting acutely injured alveolar epithelial cells in vivo while reinstating apoptotic signaling in EMT‐adapted A549 and MEF cells in vitro. Thus, targeting HSP27 may offer a promising therapeutic strategy to restore apoptotic–fibrotic equilibrium in silicosis and related pulmonary fibrotic disorders.",
  "abstract_shown": true,
  "affiliations": [
    "School of Basic Medical Sciences North China University of Science and Technology Tangshan China",
    "Hebei Key Laboratory for Chronic Diseases North China University of Science and Technology Tangshan China",
    "Department of Breast Surgery Tangshan Central Hospital Tangshan Hebei China",
    "Department of Clinical Laboratory The Third Central Hospital of Tianjin (Tianjin University Central Hospital) Tianjin China",
    "Department of Research Management Yutian County Hospital of Traditional Chinese Medicine Tangshan China",
    "Department of Clinical Microbiology Hospital of North China University of Science and Technology Tangshan China"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 14,
  "authors": [
    {
      "affs": [
        0,
        1
      ],
      "name": "Wenxin Guo"
    },
    {
      "affs": [
        2
      ],
      "name": "Jinyin Yan"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Wenli Li"
    },
    {
      "affs": [
        3
      ],
      "name": "Jin Wang"
    },
    {
      "affs": [
        4
      ],
      "name": "Lu Liu"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Chengmei Zhang"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Wei Cao"
    },
    {
      "affs": [
        5
      ],
      "name": "Shanshan Yao"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Haibo Gong"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Yi He"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Zihan Zhou"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Siyan Chen"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Li Feng"
    },
    {
      "affs": [
        0,
        1
      ],
      "name": "Haijing Deng",
      "orcid": "0009-0001-4292-6456"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/1b7c7sfz8smqq.bib",
  "cited_by": 0,
  "doi": "10.1002/ame2.70272",
  "fulltext_url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC13444399/",
  "id": "1b7c7sfz8smqq",
  "issns": [
    "2096-5451",
    "2576-2095"
  ],
  "landing_url": "https://doi.org/10.1002/ame2.70272",
  "language": "en",
  "licence": "CC-BY-NC-ND-4.0",
  "licence_label": "CC BY-NC-ND 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Original Article"
    ],
    [
      "heading",
      "Themed Section: Animal Models of Pulmonary Diseases"
    ],
    [
      "openalex",
      "2740|Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis"
    ]
  ],
  "openalex": "W7196943571",
  "pdf_url": null,
  "pmcid": "PMC13444399",
  "pmid": "42557962",
  "published": "2026-08-06",
  "publisher": "Wiley",
  "ris": "https://research.draconitic.com/paper/1b7c7sfz8smqq.ris",
  "sources": [
    {
      "first_seen": "2026-10-31T12:23:42Z",
      "native_id": "PMC13444399",
      "source": "pmc",
      "url": "https://doi.org/10.1002/ame2.70272"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2740|Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis",
      "subfield": "general"
    }
  ],
  "title": "Ac‐SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes",
  "title_text": "Ac‐SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes",
  "type": "peer-reviewed",
  "updated_at": "2026-11-01T12:20:49Z",
  "url": "https://research.draconitic.com/paper/1b7c7sfz8smqq",
  "venue": "Animal Models and Experimental Medicine",
  "versions": []
}