{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T17:40:28Z","timestamp":1791394828596,"version":"4.3.3"},"reference-count":118,"publisher":"MDPI AG","issue":"24","license":[{"start":{"date-parts":[[2024,12,18]],"date-time":"2024-12-18T00:00:00Z","timestamp":1734480000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Hutchinson\u2013Gilford progeria syndrome (HGPS) is a pediatric condition characterized by clinical features that resemble accelerated aging. The abnormal accumulation of a toxic form of the lamin A protein known as progerin disrupts cellular functions, leading to various complications, including growth retardation, loss of subcutaneous fat, abnormal skin, alopecia, osteoporosis, and progressive joint contractures. Death primarily occurs as the result of complications from progressive atherosclerosis, especially from cardiac disease, such as myocardial infarction or heart failure, or cerebrovascular disease like stroke. Despite the availability of lonafarnib, the only US Food and Drug Administration-approved treatment for HGPS, cardiovascular complications remain the leading cause of morbidity and mortality in affected patients. Defective angiogenesis\u2014the process of forming new blood vessels from existing ones\u2014plays a crucial role in the development of cardiovascular disease. A recent study suggests that Angiopoietin-2 (Ang2), a pro-angiogenic growth factor that regulates angiogenesis and vascular stability, may offer therapeutic potential for the treatment of HGPS. In this review, we describe the clinical features and key cellular processes impacted by progerin and discuss the therapeutic potential of Ang2 in addressing these challenges.<\/jats:p>","DOI":"10.3390\/ijms252413537","type":"journal-article","created":{"date-parts":[[2024,12,18]],"date-time":"2024-12-18T03:40:56Z","timestamp":1734493256000},"page":"13537","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Angiopoietin-2: A Therapeutic Target for Vascular Protection in Hutchinson\u2013Gilford Progeria Syndrome"],"prefix":"10.3390","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2285-3288","authenticated-orcid":false,"given":"Sahar","family":"Vakili","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kan","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,12,18]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"293","DOI":"10.1038\/nature01629","article-title":"Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome","volume":"423","author":"Eriksson","year":"2003","journal-title":"Nature"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"2055","DOI":"10.1126\/science.1084125","article-title":"Lamin a truncation in Hutchinson-Gilford progeria","volume":"300","author":"Bernard","year":"2003","journal-title":"Science"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"533","DOI":"10.1111\/acel.12070","article-title":"Hutchinson-Gilford progeria syndrome through the lens of transcription","volume":"12","author":"Prokocimer","year":"2013","journal-title":"Aging Cell"},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"2301","DOI":"10.1161\/ATVBAHA.110.209460","article-title":"Cardiovascular pathology in Hutchinson-Gilford progeria: Correlation with the vascular pathology of aging","volume":"30","author":"Olive","year":"2010","journal-title":"Arterioscler. 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