摘要
Klotho蛋白缺乏涉及早衰已为人所知。作为老化抑制剂,Klotho是老化进程中的一个重要的分子且其过度表达导致长寿。由于诸多原因,胰岛素/胰岛素样生长因子1(IGF-1)被认为是老化研究的关键通路。Klotho基因与这一通路联系紧密。Klotho基因编码跨膜蛋白切割后也被发现作为分泌蛋白。重要的是,其过度表达抑制胰岛素/IGF-1信号,从而延长了寿命。另外,Klotho参与一些其他胞内信号通路的调节,包括FGF23信号调节、cAMP、PKC、转化生长因子β(TGF-β)、p53/p21和Wnt信号。这篇文章的目的是总结显示Klotho参与一些胞内通路调节的现有文献。我们的综述结果清楚的表明Klotho参与一些胞内信号通路,并且通过调节它们,来参与衰老和长寿过程。
关键词: cAMP,成纤维细胞生长因子(FGF),胰岛素/IGF-1,Klotho,PKC,PTH,维生素D,p53/p21,Wnt信号通路
Current Molecular Medicine
Title:Intracellular Signaling of the Aging Suppressor Protein Klotho
Volume: 15 Issue: 1
Author(s): M. Sopjani, M. Rinnerthaler, J. Kruja and M. Dermaku-Sopjani
Affiliation:
关键词: cAMP,成纤维细胞生长因子(FGF),胰岛素/IGF-1,Klotho,PKC,PTH,维生素D,p53/p21,Wnt信号通路
摘要: The Klotho protein deficiency is known to participate in premature aging. As an aging suppressor, Klotho is an important molecule in aging processes and its overexpression results in longevity. Due to many reasons, the insulin/insulin-like growth factor-1 (IGF-1) has been considered as a key pathway in aging research. The Klotho gene is closely related to this pathway. The Klotho gene encodes a transmembrane protein that after cleavage is also found as a secreted protein. Importantly, its overexpression suppresses insulin/IGF-1 signaling and thus extends the lifespan. In addition, Klotho participates in the regulation of several other intracellular signaling pathways, including regulation of FGF23 signaling, cAMP, PKC, transforming growth factor-β (TGF-β), p53/p21, and Wnt signaling. The aim of this review is to summarize current literature that shows the involvement of Klotho in the regulation of several intracellular pathways. The results of our review clearly indicate that Klotho participates in several intracellular signaling pathways, and by regulating them, Klotho is involved in aging and longevity.
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Cite this article as:
M. Sopjani, M. Rinnerthaler, J. Kruja and M. Dermaku-Sopjani , Intracellular Signaling of the Aging Suppressor Protein Klotho, Current Molecular Medicine 2015; 15 (1) . https://dx.doi.org/10.2174/1566524015666150114111258
DOI https://dx.doi.org/10.2174/1566524015666150114111258 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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