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Roles of FGF signaling in stem cell self-renewal, senescence and aging

The aging process decreases tissue function and regenerative capacity, which has been associated with cellular senescence and a decline in adult or somatic stem cell numbers and self-renewal within multiple tissues. The potential therapeutic application of stem cells to reduce the burden of aging an...

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Autores principales: Coutu, Daniel L., Galipeau, Jacques
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229969/
https://www.ncbi.nlm.nih.gov/pubmed/21990129
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author Coutu, Daniel L.
Galipeau, Jacques
author_facet Coutu, Daniel L.
Galipeau, Jacques
author_sort Coutu, Daniel L.
collection PubMed
description The aging process decreases tissue function and regenerative capacity, which has been associated with cellular senescence and a decline in adult or somatic stem cell numbers and self-renewal within multiple tissues. The potential therapeutic application of stem cells to reduce the burden of aging and stimulate tissue regeneration after trauma is very promising. Much research is currently ongoing to identify the factors and molecular mediators of stem cell self-renewal to reach these goals. Over the last two decades, fibroblast growth factors (FGFs) and their receptors (FGFRs) have stood up as major players in both embryonic development and tissue repair. Moreover, many studies point to somatic stem cells as major targets of FGF signaling in both tissue homeostasis and repair. FGFs appear to promote self-renewing proliferation and inhibit cellular senescence in nearly all tissues tested to date. Here we review the role of FGFs and FGFRs in stem cell self-renewal, cellular senescence, and aging.
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spelling pubmed-32299692011-12-05 Roles of FGF signaling in stem cell self-renewal, senescence and aging Coutu, Daniel L. Galipeau, Jacques Aging (Albany NY) Research Perspective The aging process decreases tissue function and regenerative capacity, which has been associated with cellular senescence and a decline in adult or somatic stem cell numbers and self-renewal within multiple tissues. The potential therapeutic application of stem cells to reduce the burden of aging and stimulate tissue regeneration after trauma is very promising. Much research is currently ongoing to identify the factors and molecular mediators of stem cell self-renewal to reach these goals. Over the last two decades, fibroblast growth factors (FGFs) and their receptors (FGFRs) have stood up as major players in both embryonic development and tissue repair. Moreover, many studies point to somatic stem cells as major targets of FGF signaling in both tissue homeostasis and repair. FGFs appear to promote self-renewing proliferation and inhibit cellular senescence in nearly all tissues tested to date. Here we review the role of FGFs and FGFRs in stem cell self-renewal, cellular senescence, and aging. Impact Journals LLC 2011-10-09 /pmc/articles/PMC3229969/ /pubmed/21990129 Text en Copyright: © 2011 Coutu and Galipeau http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
spellingShingle Research Perspective
Coutu, Daniel L.
Galipeau, Jacques
Roles of FGF signaling in stem cell self-renewal, senescence and aging
title Roles of FGF signaling in stem cell self-renewal, senescence and aging
title_full Roles of FGF signaling in stem cell self-renewal, senescence and aging
title_fullStr Roles of FGF signaling in stem cell self-renewal, senescence and aging
title_full_unstemmed Roles of FGF signaling in stem cell self-renewal, senescence and aging
title_short Roles of FGF signaling in stem cell self-renewal, senescence and aging
title_sort roles of fgf signaling in stem cell self-renewal, senescence and aging
topic Research Perspective
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229969/
https://www.ncbi.nlm.nih.gov/pubmed/21990129
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