{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T16:16:30Z","timestamp":1753892190462,"version":"3.41.2"},"reference-count":28,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,11,6]],"date-time":"2024-11-06T00:00:00Z","timestamp":1730851200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000051","name":"National Human Genome Research Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000051","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Physiol."],"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p>Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic condition characterized by premature aging, impacting multiple organ systems, including cardiovascular, musculoskeletal, and integumentary. Significant abnormalities in a transgenic mouse model (homozygous G608G mutation), specifically targeting the development of skull and facial bone indices through high-resolution CT scanning and cephalometric analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Key measurements include bone thickness, skull volume, and cranial suture integrity. Bone volume increased significantly in HGPS mice by 8 months of age compared to wildtype mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Cortical thickness showed a trend toward increased values in HGPS mice. Cranial metrics revealed distinct differences.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>HGPS mice exhibited smaller internasal width, interzygomatic distance, and palatine length compared to WT mice over time.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fphys.2024.1481985","type":"journal-article","created":{"date-parts":[[2024,11,6]],"date-time":"2024-11-06T06:12:17Z","timestamp":1730873537000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Characterization of the craniofacial abnormalities of the homozygous G608G progeria mouse model"],"prefix":"10.3389","volume":"15","author":[{"given":"Indeevar","family":"Beeram","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria Belen","family":"Cubria","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pramod","family":"Kamalapathy","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diana","family":"Yeritsyan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amanda J.","family":"Dubose","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ahmad Hedayatzadeh","family":"Razavi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nazanin","family":"Nafisi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael R.","family":"Erdos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brian D.","family":"Snyder","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wayne A.","family":"Cabral","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Francis S.","family":"Collins","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ara","family":"Nazarian","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2024,11,6]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"13049","DOI":"10.1073\/pnas.192460799","article-title":"Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect","volume":"99","author":"Bergo","year":"2002","journal-title":"Proc. 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