Genomic instability in the naturally and prematurely aged myocardium

Medientyp: E-Artikel
Titel: Genomic instability in the naturally and prematurely aged myocardium
Beteiligte: De Majo, Federica; Martens, Leonie; Hegenbarth, Jana-Charlotte; Rühle, Frank; Hamczyk, Magda R.; Nevado, Rosa M.; Andrés, Vicente; Hilbold, Erika; Bär, Christian; Thum, Thomas; de Boer, Martine; Duncker, Dirk J.; Schroen, Blanche; Armand, Anne-Sophie; Stoll, Monika; De Windt, Leon J.
Erschienen: Proceedings of the National Academy of Sciences, 2021
Erschienen in: Proceedings of the National Academy of Sciences
Sprache: Englisch
DOI: 10.1073/pnas.2022974118
ISSN: 0027-8424; 1091-6490
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Beschreibung: <jats:title>Significance</jats:title><jats:p>Accumulation of DNA variants is considered a cause of organ dysfunction during natural aging. Here, we directly assessed the frequency of DNA damage of the murine myocardium during natural aging and in hearts from four mouse models of premature aging. In contrast to the prevailing dogma, our results provide no evidence for an enrichment in variants in the naturally aging heart until 2 y of age in Hutchinson–Gilford Progeria Syndrome hearts or in hearts with reduced telomere lengths. Accumulation of randomly distributed variants was, however, evident in Ercc1 knockout mice with deficient DNA repair machinery and in the intestine, liver, and lung of naturally aging mice. These results launch avenues to dissect the fundamental biological processes underlying cardiac aging.</jats:p>
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