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Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging.
Das, Abhirup; Huang, George X; Bonkowski, Michael S; Longchamp, Alban; Li, Catherine; Schultz, Michael B; Kim, Lynn-Jee; Osborne, Brenna; Joshi, Sanket; Lu, Yuancheng; Treviño-Villarreal, Jose Humberto; Kang, Myung-Jin; Hung, Tzong-Tyng; Lee, Brendan; Williams, Eric O; Igarashi, Masaki; Mitchell, James R; Wu, Lindsay E; Turner, Nigel; Arany, Zolt; Guarente, Leonard; Sinclair, David A.
Afiliação
  • Das A; Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia; Paul F. Glenn Ce
  • Huang GX; Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Cardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Boulevard, Bldg. 421, Philadelphia, PA 19104, USA.
  • Bonkowski MS; Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
  • Longchamp A; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Li C; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Schultz MB; Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
  • Kim LJ; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Osborne B; Mitochondrial Bioenergetics Laboratory, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Joshi S; Mitochondrial Bioenergetics Laboratory, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Lu Y; Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
  • Treviño-Villarreal JH; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Kang MJ; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Hung TT; Biological Resources Imaging Laboratory, Mark Wainwright Analytical Centre, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Lee B; Biological Resources Imaging Laboratory, Mark Wainwright Analytical Centre, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Williams EO; Paul F. Glenn Center for Science of Aging Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Igarashi M; Paul F. Glenn Center for Science of Aging Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Mitchell JR; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Wu LE; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Turner N; Mitochondrial Bioenergetics Laboratory, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
  • Arany Z; Cardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Boulevard, Bldg. 421, Philadelphia, PA 19104, USA. Electronic address: zarany@pennmedicine.upenn.edu.
  • Guarente L; Paul F. Glenn Center for Science of Aging Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: leng@mit.edu.
  • Sinclair DA; Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia. Electronic addre
Cell ; 173(1): 74-89.e20, 2018 03 22.
Article em En | MEDLINE | ID: mdl-29570999
A decline in capillary density and blood flow with age is a major cause of mortality and morbidity. Understanding why this occurs is key to future gains in human health. NAD precursors reverse aspects of aging, in part, by activating sirtuin deacylases (SIRT1-SIRT7) that mediate the benefits of exercise and dietary restriction (DR). We show that SIRT1 in endothelial cells is a key mediator of pro-angiogenic signals secreted from myocytes. Treatment of mice with the NAD+ booster nicotinamide mononucleotide (NMN) improves blood flow and increases endurance in elderly mice by promoting SIRT1-dependent increases in capillary density, an effect augmented by exercise or increasing the levels of hydrogen sulfide (H2S), a DR mimetic and regulator of endothelial NAD+ levels. These findings have implications for improving blood flow to organs and tissues, increasing human performance, and reestablishing a virtuous cycle of mobility in the elderly.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Envelhecimento / Sulfeto de Hidrogênio / NAD Limite: Animals / Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Envelhecimento / Sulfeto de Hidrogênio / NAD Limite: Animals / Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article