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The mTORC1-autophagy pathway is a target for senescent cell elimination

Cellular senescence has recently been established as a key driver of organismal ageing. The state of senescence is controlled by extensive rewiring of signalling pathways, at the heart of which lies the mammalian Target of Rapamycin Complex I (mTORC1). Here we discuss recent publications aiming to e...

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Autores principales: Kucheryavenko, Olena, Nelson, Glyn, von Zglinicki, Thomas, Korolchuk, Viktor I., Carroll, Bernadette
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535413/
https://www.ncbi.nlm.nih.gov/pubmed/30798505
http://dx.doi.org/10.1007/s10522-019-09802-9
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author Kucheryavenko, Olena
Nelson, Glyn
von Zglinicki, Thomas
Korolchuk, Viktor I.
Carroll, Bernadette
author_facet Kucheryavenko, Olena
Nelson, Glyn
von Zglinicki, Thomas
Korolchuk, Viktor I.
Carroll, Bernadette
author_sort Kucheryavenko, Olena
collection PubMed
description Cellular senescence has recently been established as a key driver of organismal ageing. The state of senescence is controlled by extensive rewiring of signalling pathways, at the heart of which lies the mammalian Target of Rapamycin Complex I (mTORC1). Here we discuss recent publications aiming to establish the mechanisms by which mTORC1 drives the senescence program. In particular, we highlight our data indicating that mTORC1 can be used as a target for senescence cell elimination in vitro. Suppression of mTORC1 is known to extend lifespan of yeast, worms, flies and some mouse models and our proof-of-concept experiments suggest that it can also act by reducing senescent cell load in vivo.
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spelling pubmed-65354132019-06-12 The mTORC1-autophagy pathway is a target for senescent cell elimination Kucheryavenko, Olena Nelson, Glyn von Zglinicki, Thomas Korolchuk, Viktor I. Carroll, Bernadette Biogerontology Research Article Cellular senescence has recently been established as a key driver of organismal ageing. The state of senescence is controlled by extensive rewiring of signalling pathways, at the heart of which lies the mammalian Target of Rapamycin Complex I (mTORC1). Here we discuss recent publications aiming to establish the mechanisms by which mTORC1 drives the senescence program. In particular, we highlight our data indicating that mTORC1 can be used as a target for senescence cell elimination in vitro. Suppression of mTORC1 is known to extend lifespan of yeast, worms, flies and some mouse models and our proof-of-concept experiments suggest that it can also act by reducing senescent cell load in vivo. Springer Netherlands 2019-02-23 2019 /pmc/articles/PMC6535413/ /pubmed/30798505 http://dx.doi.org/10.1007/s10522-019-09802-9 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Research Article
Kucheryavenko, Olena
Nelson, Glyn
von Zglinicki, Thomas
Korolchuk, Viktor I.
Carroll, Bernadette
The mTORC1-autophagy pathway is a target for senescent cell elimination
title The mTORC1-autophagy pathway is a target for senescent cell elimination
title_full The mTORC1-autophagy pathway is a target for senescent cell elimination
title_fullStr The mTORC1-autophagy pathway is a target for senescent cell elimination
title_full_unstemmed The mTORC1-autophagy pathway is a target for senescent cell elimination
title_short The mTORC1-autophagy pathway is a target for senescent cell elimination
title_sort mtorc1-autophagy pathway is a target for senescent cell elimination
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535413/
https://www.ncbi.nlm.nih.gov/pubmed/30798505
http://dx.doi.org/10.1007/s10522-019-09802-9
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