IL-6-STAT3 signaling and premature senescence.
IL-6-STAT3 signaling and premature senescence.
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DOI：
10.4161/jkst.25763
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发表时间：
2013-10-01
期刊：
影响因子：
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通讯作者：
Nakajima K
中科院分区：
文献类型：
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作者：
Kojima H;Inoue T;Kunimoto H;Nakajima K
细胞因子在发展和/或加强年轻细胞的过早细胞衰老中起着多种作用。其中一种细胞因子，白细胞介素-6 (IL-6)，除了其已知的免疫调节和促进肿瘤发生的功能外，还调节某些系统的衰老。本文综述了IL-6及其下游信号转导因子和转录激活因子3 （STAT3）在调控细胞过早衰老中的作用。在人成纤维细胞中，IL-6/sIL-6Rα刺激形成了一个衰老诱导回路，其中stat3 -胰岛素样生长因子结合蛋白5 （IGFBP5）是一个关键的轴触发和增强成分。我们描述了细胞因子如何通过激活一个系统中的STAT3和在其他系统中的抗衰老或肿瘤发生来调节衰老过程。其他STAT成员在过早衰老中的作用也将被讨论，以显示导致细胞因子诱导衰老的多种机制。
Cytokines play several roles in developing and/or reinforcing premature cellular senescence of young cells. One such cytokine, interleukin-6 (IL-6), regulates senescence in some systems in addition to its known functions of immune regulation and promotion of tumorigenesis. In this review, we describe recent advances in studies on the roles of IL-6 and its downstream signal transducer and activator of transcription 3 (STAT3) in regulating premature cellular senescence. IL-6/sIL-6Rα stimulation forms a senescence-inducing circuit involving the STAT3-insulin-like growth factor-binding protein 5 (IGFBP5) as a key axis triggering and reinforcing component in human fibroblasts. We describe how cytokines regulate the process of senescence by activating STAT3 in one system and anti-senescence or tumorigenesis in other systems. The roles of other STAT members in premature senescence also will be discussed to show the multiple mechanisms leading to cytokine-induced senescence.