2026-06-14T05:17:51Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/78692024-11-29T22:37:15Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Nóbrega-Pereira, Sandrina
author
Fernandez-Marcos, Pablo J
author
Brioche, Thomas
author
Gomez-Cabrera, Mari Carmen
author
Salvador-Pascual, Andrea
author
Flores, Juana M
author
Viña, Jose
author
Serrano Marugan, Manuel
funder
Asociación Española Contra el Cáncer
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Botín Foundation
funder
Fundación AXA
funder
Banco Santander
funder
Fundación Ramón Areces
2019-07-08T11:31:51Z
2019-07-08T11:31:51Z
2016-03-15
Nat Commun. 2016;7:11739
10.1038/ncomms10894
2041-1723
2041-1723
Nature communications
26976705
http://hdl.handle.net/20.500.12105/7869
Reactive oxygen species (ROS) are constantly generated by cells and ROS-derived damage contributes to ageing. Protection against oxidative damage largely relies on the reductive power of NAPDH, whose levels are mostly determined by the enzyme glucose-6-phosphate dehydrogenase (G6PD). Here, we report a transgenic mouse model with moderate overexpression of human G6PD under its endogenous promoter. Importantly, G6PD-Tg mice have higher levels of NADPH, lower levels of ROS-derived damage, and better protection from ageing-associated functional decline, including extended median lifespan in females. The G6PD transgene has no effect on tumour development, even after combining with various tumour-prone genetic alterations. We conclude that a modest increase in G6PD activity is beneficial for healthspan through increased NADPH levels and protection from the deleterious effects of ROS.
eng
G6PD protects from oxidative damage and improves healthspan in mice
journal article
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