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Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging

The global population aging is accelerating and age-associated diseases including cardiovascular diseases become more challenging. The underlying mechanisms of aging and age-associated cardiovascular dysfunction remain elusive. There are substantial evidences demonstrating a pivotal role of the mamm...

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Detalles Bibliográficos
Autores principales: Ming, Xiu-Fen, Montani, Jean-Pierre, Yang, Zhihong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3265748/
https://www.ncbi.nlm.nih.gov/pubmed/22291661
http://dx.doi.org/10.3389/fphys.2012.00005
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author Ming, Xiu-Fen
Montani, Jean-Pierre
Yang, Zhihong
author_facet Ming, Xiu-Fen
Montani, Jean-Pierre
Yang, Zhihong
author_sort Ming, Xiu-Fen
collection PubMed
description The global population aging is accelerating and age-associated diseases including cardiovascular diseases become more challenging. The underlying mechanisms of aging and age-associated cardiovascular dysfunction remain elusive. There are substantial evidences demonstrating a pivotal role of the mammalian target of rapamycin complex 1 (mTORC1) and its down-stream effector S6K1 signaling in mammalian lifespan regulation and age-related diseases such as type II diabetes mellitus and cancer. The role of mTORC1–S6K1 in age-related cardiovascular diseases is, however, largely unknown and the available experimental results are controversial. This review article primarily summarizes the most recent advances toward understanding the role of mTORC1–S6K1 in cardiovascular aging and discusses the future perspectives of targeting mTORC1–S6K1 signaling as a healthy lifespan extension modality in anti-aging and anti-cardiovascular aging.
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spelling pubmed-32657482012-01-30 Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging Ming, Xiu-Fen Montani, Jean-Pierre Yang, Zhihong Front Physiol Physiology The global population aging is accelerating and age-associated diseases including cardiovascular diseases become more challenging. The underlying mechanisms of aging and age-associated cardiovascular dysfunction remain elusive. There are substantial evidences demonstrating a pivotal role of the mammalian target of rapamycin complex 1 (mTORC1) and its down-stream effector S6K1 signaling in mammalian lifespan regulation and age-related diseases such as type II diabetes mellitus and cancer. The role of mTORC1–S6K1 in age-related cardiovascular diseases is, however, largely unknown and the available experimental results are controversial. This review article primarily summarizes the most recent advances toward understanding the role of mTORC1–S6K1 in cardiovascular aging and discusses the future perspectives of targeting mTORC1–S6K1 signaling as a healthy lifespan extension modality in anti-aging and anti-cardiovascular aging. Frontiers Research Foundation 2012-01-25 /pmc/articles/PMC3265748/ /pubmed/22291661 http://dx.doi.org/10.3389/fphys.2012.00005 Text en Copyright © 2012 Ming, Montani and Yang. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
spellingShingle Physiology
Ming, Xiu-Fen
Montani, Jean-Pierre
Yang, Zhihong
Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging
title Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging
title_full Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging
title_fullStr Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging
title_full_unstemmed Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging
title_short Perspectives of Targeting mTORC1–S6K1 in Cardiovascular Aging
title_sort perspectives of targeting mtorc1–s6k1 in cardiovascular aging
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3265748/
https://www.ncbi.nlm.nih.gov/pubmed/22291661
http://dx.doi.org/10.3389/fphys.2012.00005
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