{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T07:38:10Z","timestamp":1792568290252,"version":"4.5.0"},"reference-count":61,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T00:00:00Z","timestamp":1792454400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T00:00:00Z","timestamp":1792454400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["P01AG066591"],"award-info":[{"award-number":["P01AG066591"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["T32AG052374"],"award-info":[{"award-number":["T32AG052374"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002347","name":"Bundesministerium f\u00fcr Forschung, Technologie und Raumfahrt","doi-asserted-by":"publisher","award":["13N15745"],"award-info":[{"award-number":["13N15745"]}],"id":[{"id":"10.13039\/501100002347","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Patients with idiopathic pulmonary fibrosis (IPF) are highly vulnerable to respiratory virus infections, but the cellular mechanisms linking fibrotic remodeling to impaired local antiviral defense remain unclear. Here, we investigated how cellular senescence shapes the response of patient\u2010derived healthy (HLF) and IPF primary lung fibroblasts to influenza A virus (IAV) infection. Transcriptomic profiling identified infection as the driver of gene expression in both DNA damage\u2010induced senescent HLF and IPF fibroblasts and revealed induction of canonical antiviral pathways in both cell states. However, senescent IPF fibroblasts adopted a distinct antiviral response state characterized by a broader set of uniquely induced genes and differential coordination of antiviral transcriptional networks. Functionally, senescence increased viral titers in HLF and IPF fibroblasts, while senescent IPF fibroblasts displayed an altered inflammatory response. Network analysis linked viral response\u2010 and cell cycle\u2010associated modules specifically to the senescent HLF infected state, whereas these programs were weaker in senescent IPF fibroblasts. Transcription factor inference identified\n                    <jats:italic>IRF3<\/jats:italic>\n                    and\n                    <jats:italic>STAT1<\/jats:italic>\n                    as candidate regulators of this altered antiviral state in both senescent HLF and IPF fibroblasts. Consistent with the network and transcription factor analyses, siRNA\u2010mediated depletion of\n                    <jats:italic>IRF3<\/jats:italic>\n                    or\n                    <jats:italic>STAT1<\/jats:italic>\n                    significantly reduced IFN\u2010\u03b2 secretion in senescent HLF fibroblasts, whereas IPF fibroblasts showed only milder effects, indicating a disease\u2010specific dependence on these pathways for antiviral control. Together, these findings show that the combination of cellular senescence and fibrotic fibroblast identity creates a dysfunctional antiviral state that may help explain the high susceptibility of IPF patients to virus\u2010associated acute exacerbations and disease worsening.\n                  <\/jats:p>","DOI":"10.1111\/acel.70763","type":"journal-article","created":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T06:40:30Z","timestamp":1792564830000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Cellular Senescence Dysregulates Antiviral Interferon Responses in Idiopathic Pulmonary Fibrosis"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1887-0242","authenticated-orcid":false,"given":"Jun\u2010Wei B.","family":"Hughes","sequence":"first","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California USA"},{"name":"Leonard Davis School of Gerontology University of Southern California  Los Angeles California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-9757-5036","authenticated-orcid":false,"given":"Yasmina","family":"Reisser","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology Jena University Hospital  Jena Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franziska","family":"Hornung","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology Jena University Hospital  Jena Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1690-4704","authenticated-orcid":false,"given":"Tyler A. U.","family":"Hilsabeck","sequence":"additional","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-3504-1269","authenticated-orcid":false,"given":"Fiona","family":"Senchyna","sequence":"additional","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana L.","family":"Coelho","sequence":"additional","affiliation":[{"name":"Cedars\u2010Sinai  Los Angeles California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tsung\u2010Che","family":"Ho","sequence":"additional","affiliation":[{"name":"University of California, San Francisco  San Francisco California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin","family":"Schneider","sequence":"additional","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3654-9519","authenticated-orcid":false,"given":"David","family":"Furman","sequence":"additional","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3366-4850","authenticated-orcid":false,"given":"Cory M.","family":"Hogaboam","sequence":"additional","affiliation":[{"name":"Cedars\u2010Sinai  Los Angeles California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6041-2870","authenticated-orcid":false,"given":"Claude Jourdan","family":"Le Saux","sequence":"additional","affiliation":[{"name":"University of California, San Francisco  San Francisco California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre\u2010Yves","family":"Desprez","sequence":"additional","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California USA"},{"name":"California Pacific Medical Center Research Institute  San Francisco California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4495-4052","authenticated-orcid":false,"given":"Stefanie","family":"Deinhardt\u2010Emmer","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology Jena University Hospital  Jena Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,20]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"crossref","DOI":"10.1093\/genetics\/iyad031","article-title":"The Gene Ontology Knowledgebase in 2023","volume":"224","author":"Aleksander S. 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