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Transcriptional Control of Endothelial Senescence and Vascular Repair

衰老 表观遗传学 生物 细胞衰老 糖尿病 老年学 医学 遗传学 内分泌学 表型 基因
作者
Assam El‐Osta
出处
期刊:Circulation Research [Lippincott Williams & Wilkins]
卷期号:133 (10): 858-860 被引量:1
标识
DOI:10.1161/circresaha.123.323716
摘要

HomeCirculation ResearchVol. 133, No. 10Transcriptional Control of Endothelial Senescence and Vascular Repair No AccessEditorialRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessEditorialRequest AccessFull TextTranscriptional Control of Endothelial Senescence and Vascular Repair Assam El-Osta Assam El-OstaAssam El-Osta Correspondence to: Assam El-Osta, PhD, Epigenetics in Human Health and Disease Program, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC 3004, Australia. Email E-mail Address: [email protected] https://orcid.org/0000-0003-2969-9137 Epigenetics in Human Health and Disease Program, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia. Originally published26 Oct 2023https://doi.org/10.1161/CIRCRESAHA.123.323716Circulation Research. 2023;133:858–860This article is a commentary on the followingDisrupted Binding of Cystathionine γ-Lyase to p53 Promotes Endothelial SenescenceFootnotesFor Sources of Funding and Disclosures, see page 860.Correspondence to: Assam El-Osta, PhD, Epigenetics in Human Health and Disease Program, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC 3004, Australia. Email sam.el-osta@baker.edu.auReferences1. Hayflick L, Moorhead PS. The serial cultivation of human diploid cell strains.Exp Cell Res. 1961; 25:585–621. doi: 10.1016/0014-4827(61)90192-6CrossrefMedlineGoogle Scholar2. Ungvari Z, Tarantini S, Donato AJ, Galvan V, Csiszar A. Mechanisms of vascular aging.Circ Res. 2018; 123:849–867. doi: 10.1161/CIRCRESAHA.118.311378LinkGoogle Scholar3. Hammadah M, Al Mheid I, Wilmot K, Ramadan R, Abdelhadi N, Alkhoder A, Obideen M, Pimple PM, Levantsevych O, Kelli HM, et al. Telomere shortening, regenerative capacity, and cardiovascular outcomes.Circ Res. 2017; 120:1130–1138. doi: 10.1161/CIRCRESAHA.116.309421LinkGoogle Scholar4. Al Mheid I, Hayek SS, Ko YA, Akbik F, Li Q, Ghasemzadeh N, Martin GS, Long Q, Hammadah M, Maziar Zafari A, et al. Age and human regenerative capacity impact of cardiovascular risk factors.Circ Res. 2016; 119:801–809. doi: 10.1161/CIRCRESAHA.116.308461LinkGoogle Scholar5. Jiong Hu MSL, Looso M, Drekolia MK, Wittig J, Mettner J, Karantanou C, Kyselova A, Dumbovic G, Li X, Li Y, et al. Disrupted binding of cystathionine 1 γ lyase to p53 promotes endothelial senescence.Circ Res. 2023; 133:842–857. doi: 10.1161/CIRCRESAHA.123.323084LinkGoogle Scholar6. Gulve N, Su C, Deng Z, Soldan SS, Vladimirova O, Wickramasinghe J, Zheng H, Kossenkov AV, Lieberman PM. DAXX-ATRX regulation of p53 chromatin binding and DNA damage response.Nat Commun. 2022; 13:5033. doi: 10.1038/s41467-022-32680-8CrossrefMedlineGoogle Scholar7. Schwartz M, Portugez AS, Attia BZ, Tannenbaum M, Cohen L, Loza O, Chase E, Turman Y, Kaplan T, Salah Z, et al. Genomic retargeting of p53 and CTCF is associated with transcriptional changes during oncogenic HRas-induced transformation.Commun Biol. 2020; 3:696. doi: 10.1038/s42003-020-01398-yCrossrefMedlineGoogle Scholar8. Rokudai S, Laptenko O, Arnal SM, Taya Y, Kitabayashi I, Prives C. MOZ increases p53 acetylation and premature senescence through its complex formation with PML.Proc Natl Acad Sci USA. 2013; 110:3895–3900. doi: 10.1073/pnas.1300490110CrossrefMedlineGoogle Scholar9. Gu W, Roeder RG. Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.Cell. 1997; 90:595–606. doi: 10.1016/s0092-8674(00)80521-8CrossrefMedlineGoogle Scholar10. Tang Y, Zhao W, Chen Y, Zhao Y, Gu W. Acetylation is indispensable for p53 activation.Cell. 2008; 133:612–626. doi: 10.1016/j.cell.2008.03.025CrossrefMedlineGoogle Scholar11. Bibli SI, Hu J, Sigala F, Wittig I, Heidler J, Zukunft S, Tsilimigras DI, Randriamboavonjy V, Wittig J, Kojonazarov B, et al. Cystathionine γ lyase sulfhydrates the RNA binding protein human antigen R to preserve endothelial cell function and delay atherogenesis.Circulation. 2019; 139:101–114. doi: 10.1161/CIRCULATIONAHA.118.034757LinkGoogle Scholar eLetters(0) eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate. Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page. Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesDisrupted Binding of Cystathionine γ-Lyase to p53 Promotes Endothelial SenescenceJiong Hu, et al. Circulation Research. 2023;133:842-857 October 27, 2023Vol 133, Issue 10 Advertisement Article Information Metrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.123.323716PMID: 37883591 Originally publishedOctober 26, 2023 KeywordsEditorialsacetylationagingcellular senescenceepigenomicsheart diseasetelomerasePDF download Advertisement
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