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成纤维细胞生长因子信号在干细胞自我更新、衰老及老化过程中的作用。

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

作者信息

Coutu Daniel L, Galipeau Jacques

机构信息

Stem Cell Dynamics Research Unit, Helmholtz Zentrum München, Munich, Germany.

出版信息

Aging (Albany NY). 2011 Oct;3(10):920-33. doi: 10.18632/aging.100369.

DOI:10.18632/aging.100369
PMID:21990129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3229969/
Abstract

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.

摘要

衰老过程会降低组织功能和再生能力,这与细胞衰老以及多个组织中成年或体细胞干细胞数量的减少和自我更新能力的下降有关。干细胞在减轻衰老负担和促进创伤后组织再生方面的潜在治疗应用前景广阔。目前正在进行大量研究,以确定实现这些目标的干细胞自我更新的因素和分子介质。在过去二十年中,成纤维细胞生长因子(FGFs)及其受体(FGFRs)已成为胚胎发育和组织修复中的主要参与者。此外,许多研究指出,体细胞干细胞是FGF信号在组织稳态和修复中的主要靶点。迄今为止,在几乎所有测试的组织中,FGFs似乎都能促进自我更新增殖并抑制细胞衰老。在此,我们综述FGFs和FGFRs在干细胞自我更新、细胞衰老和衰老中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd4/3229969/d9eb7e6c4df8/aging-03-920-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd4/3229969/64f93f70040c/aging-03-920-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd4/3229969/d9eb7e6c4df8/aging-03-920-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd4/3229969/64f93f70040c/aging-03-920-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd4/3229969/d9eb7e6c4df8/aging-03-920-g002.jpg

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