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

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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Bibliographic Details
Main Authors: 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
Format: article
Language:EN
Published: Nature Portfolio 2018
Subjects:
Science
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Online Access:https://doaj.org/article/b33496fa8a17473f945f0a89142ec415
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Summary: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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