Declining NAD( ) Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging
Ana P Gomes, Nathan L Price, Alvin JY Ling, Javid J Moslehi, Magdalene K Montgomery, Luis Rajman, James P White, Joao S Teodoro, Christiane D Wrann, Basil P Hubbard, Evi M Mercken, Carlos M Palmeira, Rafael de Cabo, Anabela P Rolo, Nigel Turner, Eric L Bell, David A Sinclair
Cell | CELL PRESS | Published : 2013
Awarded by Portuguese Foundation for Science and Technology
Awarded by NATIONAL INSTITUTE ON AGING
The Sinclair lab is supported by the NIH/NIA, the Glenn Foundation for Medical Research, the United Mitochondrial Disease Foundation, the Juvenile Diabetes Research Foundation, and a gift from the Schulak family. A. P. G. was supported by the Portuguese Foundation for Science and Technology (SFRH/BD/44674/2008) and B. P. H. by an NSERC PGS-D fellowship. N.T. is supported by an Australian Research Council Future Fellowship. We are grateful to Michael Bonkowski, Carlos Daniel de Magalhaes Filho, Meghan Rego, Nikolina Dioufa, and David Zhang for technical advice and experimental assistance; William Kaelin Jr. for kindly providing the EglN1 KO mice; Daniel Kelly, John Rumsay, and Teresa Leone for unpublished PGC-1 alpha/beta KO myoblasts and advice; Bruce Spiegelman for PGC-1 alpha null myoblasts and advice; and Pere Puigserver and Zachary Gerhart-Hines for a SIRT1 adenovirus. D. A. S. is a consultant to Cohbar, OvaScience, HorizonScience, Segterra, MetroBiotech, and GlaxoSmithKline. Cohbar, MetroBiotech, and GlaxoSmithKline work on mitochondrially derived peptides, NAD<SUP>+</SUP>, and sirtuin modulation, respectively.