Eidgenössische Technische Hochschule (ETH) Zürich, Health Sciences and Technology, Schwerzenbach, Switzerland.
Gerontology. 2018;64(1):96-104. doi: 10.1159/000480504. Epub 2017 Sep 22.
The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other genes in this pathway can double lifespan. Subsequent work has revealed that reduced IIS (rIIS) extends lifespan across diverse species, possibly including humans. In C. elegans, IIS also regulates development into the diapause state known as dauer, a quiescent larval form that enables C. elegans to endure harsh environments through morphological adaptation, improved cellular repair, and slowed metabolism. Considerable progress has been made uncovering mechanisms that are affected by C. elegans rIIS. However, from the beginning it has remained unclear to what extent rIIS extends C. elegans lifespan by mobilizing dauer-associated mechanisms in adults. As we discuss, recent work has shed light on this question by determining that rIIS can extend C. elegans lifespan comparably through downstream processes that are either dauer-related or -independent. Importantly, these two lifespan extension programs can be distinguished genetically. It will now be critical to tease apart these programs, because each may involve different longevity-promoting mechanisms that may be relevant to higher organisms. A recent analysis of organismal "healthspan" has questioned the value of C. elegans rIIS as a paradigm for understanding healthy aging, as opposed to simply extending life. We discuss other work that argues strongly that C. elegans rIIS is indeed an invaluable model and consider the likely possibility that dauer-related processes affect parameters associated with health under rIIS conditions. Together, these studies indicate that C. elegans and analyses of rIIS in this organism will continue to provide unexpected and exciting results, and new paradigms that will be valuable for understanding healthy aging in humans.
24 年前,在秀丽隐杆线虫中发现较低水平的胰岛素/胰岛素样生长因子-1 信号(IIS)可以诱导寿命延长,这是一项开创性的发现。在这个生物体中,胰岛素/胰岛素样生长因子-1 受体基因 daf-2 或该途径中的其他基因突变可以使寿命延长一倍。随后的工作表明,降低 IIS(rIIS)可以延长多种物种的寿命,可能包括人类。在秀丽隐杆线虫中,IIS 还调节进入称为 dauer 的休眠状态的发育,这是一种静止的幼虫形式,使秀丽隐杆线虫能够通过形态适应、改善细胞修复和减缓新陈代谢来忍受恶劣环境。在揭示受 rIIS 影响的机制方面已经取得了相当大的进展。然而,从一开始,rIIS 通过动员成年 dauer 相关机制来延长秀丽隐杆线虫寿命的程度就不清楚。正如我们所讨论的,最近的工作通过确定 rIIS 可以通过与 dauer 相关或不相关的下游过程来相当程度地延长秀丽隐杆线虫的寿命,从而阐明了这个问题。重要的是,这两种延长寿命的程序可以在遗传上区分开来。现在至关重要的是要区分这些程序,因为每个程序可能涉及到不同的促进长寿的机制,这些机制可能与高等生物有关。最近对生物体“健康寿命”的分析对 rIIS 作为理解健康衰老而不是简单延长寿命的典范的价值提出了质疑。我们讨论了其他一些强有力的观点,即 rIIS 确实是一个非常宝贵的模型,并考虑了 dauer 相关过程可能会影响 rIIS 条件下与健康相关的参数的可能性。这些研究表明,秀丽隐杆线虫及其在该生物体中 rIIS 的分析将继续提供意想不到和令人兴奋的结果,并为理解人类健康衰老提供新的范例。