Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome

Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related phenotypes in a mouse model of premature aging.

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Autores principales: Gabriel Balmus, Delphine Larrieu, Ana C. Barros, Casey Collins, Monica Abrudan, Mukerrem Demir, Nicola J. Geisler, Christopher J. Lelliott, Jacqueline K. White, Natasha A. Karp, James Atkinson, Andrea Kirton, Matt Jacobsen, Dean Clift, Raphael Rodriguez, Sanger Mouse Genetics Project, David J. Adams, Stephen P. Jackson
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/b33496fa8a17473f945f0a89142ec415
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spelling oai:doaj.org-article:b33496fa8a17473f945f0a89142ec4152021-12-02T17:32:01ZTargeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome10.1038/s41467-018-03770-32041-1723https://doaj.org/article/b33496fa8a17473f945f0a89142ec4152018-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-03770-3https://doaj.org/toc/2041-1723Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related phenotypes in a mouse model of premature aging.Gabriel BalmusDelphine LarrieuAna C. BarrosCasey CollinsMonica AbrudanMukerrem DemirNicola J. GeislerChristopher J. LelliottJacqueline K. WhiteNatasha A. KarpJames AtkinsonAndrea KirtonMatt JacobsenDean CliftRaphael RodriguezSanger Mouse Genetics ProjectDavid J. AdamsStephen P. JacksonNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-14 (2018)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Gabriel Balmus
Delphine Larrieu
Ana C. Barros
Casey Collins
Monica Abrudan
Mukerrem Demir
Nicola J. Geisler
Christopher J. Lelliott
Jacqueline K. White
Natasha A. Karp
James Atkinson
Andrea Kirton
Matt Jacobsen
Dean Clift
Raphael Rodriguez
Sanger Mouse Genetics Project
David J. Adams
Stephen P. Jackson
Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome
description Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related phenotypes in a mouse model of premature aging.
format article
author Gabriel Balmus
Delphine Larrieu
Ana C. Barros
Casey Collins
Monica Abrudan
Mukerrem Demir
Nicola J. Geisler
Christopher J. Lelliott
Jacqueline K. White
Natasha A. Karp
James Atkinson
Andrea Kirton
Matt Jacobsen
Dean Clift
Raphael Rodriguez
Sanger Mouse Genetics Project
David J. Adams
Stephen P. Jackson
author_facet Gabriel Balmus
Delphine Larrieu
Ana C. Barros
Casey Collins
Monica Abrudan
Mukerrem Demir
Nicola J. Geisler
Christopher J. Lelliott
Jacqueline K. White
Natasha A. Karp
James Atkinson
Andrea Kirton
Matt Jacobsen
Dean Clift
Raphael Rodriguez
Sanger Mouse Genetics Project
David J. Adams
Stephen P. Jackson
author_sort Gabriel Balmus
title Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome
title_short Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome
title_full Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome
title_fullStr Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome
title_full_unstemmed Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome
title_sort targeting of nat10 enhances healthspan in a mouse model of human accelerated aging syndrome
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/b33496fa8a17473f945f0a89142ec415
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