胰岛素与JNK：优化代谢稳态和寿命
Insulin and JNK: optimizing metabolic homeostasis and lifespan.
作者信息
Karpac Jason, Jasper Heinrich
机构信息
Department of Biology, University of Rochester, River Campus Box 270211, Rochester, NY 14627, USA.
出版信息
Trends Endocrinol Metab. 2009 Apr;20(3):100-6. doi: 10.1016/j.tem.2008.11.004. Epub 2009 Feb 27.
Abstract
Metabolic adaptation to environmental changes is crucial for the long-term survival of an organism. Signaling mechanisms that govern this adaptation thus influence lifespan. One such mechanism is the insulin/insulin-like growth factor signaling (IIS) pathway, a central regulator of metabolism in metazoans. Recent studies have identified the stress-responsive Jun-N-terminal kinase (JNK) pathway as a regulator of IIS signaling, providing a link between environmental challenges and metabolic regulation. JNK inhibits IIS activity and, thus, promotes lifespan extension and stress tolerance. Interestingly, this interaction is also at the center of age-related metabolic diseases. Here, we review recent advances illuminating the mechanisms of the JNK-IIS interaction and its implications for metabolic diseases and lifespan in metazoans.
摘要
代谢对环境变化的适应对于生物体的长期生存至关重要。调控这种适应的信号机制因此会影响寿命。胰岛素/胰岛素样生长因子信号传导（IIS）途径就是这样一种机制，它是后生动物新陈代谢的核心调节因子。最近的研究已确定应激反应性Jun氨基末端激酶（JNK）途径是IIS信号传导的调节因子，为环境挑战与代谢调节之间提供了联系。JNK抑制IIS活性，从而促进寿命延长和应激耐受性。有趣的是，这种相互作用也是与年龄相关的代谢疾病的核心。在这里，我们综述了阐明JNK-IIS相互作用机制及其对后生动物代谢疾病和寿命影响的最新进展。
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