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Children with HGPS typically pass away in their teenage years due to cardiovascular diseases such as atherosclerosis, myocardial infarction, heart failure, and stroke. In this study, we characterized the G608G HGPS mouse model and explored cardiac and skeletal muscle function, along with senescence\u2010associated phenotypes in fibroblasts. Homozygous G608G HGPS mice exhibited cardiac dysfunction, including decreased cardiac output and stroke volume, and impaired left ventricle relaxation. Additionally, skeletal muscle exhibited decreased isometric tetanic torque, muscle atrophy, and increased fibrosis. HGPS fibroblasts showed nuclear abnormalities, decreased proliferation, and increased expression of senescence markers. These findings provide insights into the pathophysiology of the G608G HGPS mouse model and inform potential therapeutic strategies for HGPS.<\/jats:p>","DOI":"10.1111\/acel.14259","type":"journal-article","created":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T01:40:26Z","timestamp":1720057226000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Cardiac and skeletal muscle manifestations in the G608G mouse model of Hutchinson\u2010Gilford progeria syndrome"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8071-8183","authenticated-orcid":false,"given":"Yeojin","family":"Hong","sequence":"first","affiliation":[{"name":"Smidt Heart Institute Cedars\u2010Sinai Medical Center  Los Angeles California 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