{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T05:21:01Z","timestamp":1790659261209,"version":"4.1.0"},"reference-count":105,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2023,5,9]],"date-time":"2023-05-09T00:00:00Z","timestamp":1683590400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Deutsche Forschungsgemeinschaft","award":["#646337"],"award-info":[{"award-number":["#646337"]}]},{"name":"Deutsche Forschungsgemeinschaft","award":["#66527"],"award-info":[{"award-number":["#66527"]}]},{"name":"Deutsche Forschungsgemeinschaft","award":["PRF-2022-82"],"award-info":[{"award-number":["PRF-2022-82"]}]},{"DOI":"10.13039\/100002287","name":"Progeria Research Foundation","doi-asserted-by":"publisher","award":["#646337"],"award-info":[{"award-number":["#646337"]}],"id":[{"id":"10.13039\/100002287","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002287","name":"Progeria Research Foundation","doi-asserted-by":"publisher","award":["#66527"],"award-info":[{"award-number":["#66527"]}],"id":[{"id":"10.13039\/100002287","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002287","name":"Progeria Research Foundation","doi-asserted-by":"publisher","award":["PRF-2022-82"],"award-info":[{"award-number":["PRF-2022-82"]}],"id":[{"id":"10.13039\/100002287","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Hutchinson\u2013Gilford progeria syndrome (HGPS) is a rare genetic disease that causes premature aging symptoms, such as vascular diseases, lipodystrophy, loss of bone mineral density, and alopecia. HGPS is mostly linked to a heterozygous and de novo mutation in the LMNA gene (c.1824 C &gt; T; p.G608G), resulting in the production of a truncated prelamin A protein called \u201cprogerin\u201d. Progerin accumulation causes nuclear dysfunction, premature senescence, and apoptosis. Here, we examined the effects of baricitinib (Bar), an FDA-approved JAK\/STAT inhibitor, and a combination of Bar and lonafarnib (FTI) treatment on adipogenesis using skin-derived precursors (SKPs). We analyzed the effect of these treatments on the differentiation potential of SKPs isolated from pre-established human primary fibroblast cultures. Compared to mock-treated HGPS SKPs, Bar and Bar + FTI treatments improved the differentiation of HGPS SKPs into adipocytes and lipid droplet formation. Similarly, Bar and Bar + FTI treatments improved the differentiation of SKPs derived from patients with two other lipodystrophic diseases: familial partial lipodystrophy type 2 (FPLD2) and mandibuloacral dysplasia type B (MADB). Overall, the results show that Bar treatment improves adipogenesis and lipid droplet formation in HGPS, FPLD2, and MADB, indicating that Bar + FTI treatment might further ameliorate HGPS pathologies compared to lonafarnib treatment alone.<\/jats:p>","DOI":"10.3390\/cells12101350","type":"journal-article","created":{"date-parts":[[2023,5,10]],"date-time":"2023-05-10T01:40:02Z","timestamp":1683682802000},"page":"1350","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Impact of Combined Baricitinib and FTI Treatment on Adipogenesis in Hutchinson\u2013Gilford Progeria Syndrome and Other Lipodystrophic Laminopathies"],"prefix":"10.3390","volume":"12","author":[{"given":"Ramona","family":"Hartinger","sequence":"first","affiliation":[{"name":"Epigenetics of Aging, Department of Dermatology and Allergy, TUM School of Medicine, Munich Institute of Biomedical Engineering (MIBE), Technical University of Munich (TUM), 85748 Garching, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1220-1040","authenticated-orcid":false,"given":"Eva-Maria","family":"Lederer","sequence":"additional","affiliation":[{"name":"Epigenetics of Aging, Department of Dermatology and Allergy, TUM School of Medicine, Munich Institute of Biomedical Engineering (MIBE), Technical University of Munich (TUM), 85748 Garching, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisa","family":"Schena","sequence":"additional","affiliation":[{"name":"Unit of Bologna, CNR Institute of Molecular Genetics \u201cLuigi Luca Cavalli-Sforza\u201d, 40136 Bologna, Italy"},{"name":"IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7103-8722","authenticated-orcid":false,"given":"Giovanna","family":"Lattanzi","sequence":"additional","affiliation":[{"name":"Unit of Bologna, CNR Institute of Molecular Genetics \u201cLuigi Luca Cavalli-Sforza\u201d, 40136 Bologna, Italy"},{"name":"IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4067-4977","authenticated-orcid":false,"given":"Karima","family":"Djabali","sequence":"additional","affiliation":[{"name":"Epigenetics of Aging, Department of Dermatology and Allergy, TUM School of Medicine, Munich Institute of Biomedical Engineering (MIBE), Technical University of Munich (TUM), 85748 Garching, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,5,9]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1687","DOI":"10.1001\/jama.2018.3264","article-title":"Association of Lonafarnib Treatment vs. No Treatment with Mortality Rate in Patients with Hutchinson-Gilford Progeria Syndrome","volume":"319","author":"Gordon","year":"2018","journal-title":"JAMA"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"592","DOI":"10.1056\/NEJMoa0706898","article-title":"Phenotype and course of Hutchinson-Gilford progeria syndrome","volume":"358","author":"Merideth","year":"2008","journal-title":"N. 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