抗衰老酶的发现提高了寿命延长的前景

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Anti-aging enzyme discovery raises prospect of lifespan extension

New research has shed light on an enzyme that has been linked to longer lifespan

New research has shed light on an enzyme that has been linked to longer lifespan 新的研究揭示了一种与长寿有关的酶
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A study from researchers at KAIST (Korea Advanced Institute of Science and Technology) is providing new insights into a cellular energy pathway that has been linked to longer lifespan. The research, conducted in human cells and roundworms, raises the prospect of anti-aging therapeutics that can extend lifespan by activating this pathway.

韩国科学技术高等研究院(KAIST)的研究人员的一项研究为细胞能量通路提供了新的见解,该通路与更长的寿命有关。这项在人类细胞和蛔虫中进行的研究,提高了通过激活这一途径延长寿命的抗衰老疗法的前景。

AMPK (adenosine monophosphate-activated protein kinase) is an enzyme that acts as a metabolic master switch. It has been described as a “magic bullet” protein, conferring broad beneficial health effects, from improving cardiovascular health to extending lifespan. It is activated in response to low cellular energy levels, as is often seen during exercise or periods of caloric restriction.

AMPK (AMP活化蛋白激酶)是一种酶,作为代谢的主开关。它被描述为一种“魔术子弹”蛋白质,赋予从改善心血管健康到延长寿命的广泛的有益健康作用。它是在细胞能量水平低的时候被激活的,就像经常在运动或限制热量时看到的那样。


An increasing volume of study has found activating AMPK in animal models leads to notable increases in lifespan, prompting a surge in research investigating this enzyme.

越来越多的研究发现,在动物模型中激活 AMPK 可以显著延长寿命,促进了对这种酶的研究。

The new KAIST study focused on this pathway in a tiny roundworm, caenorhabditis elegans (C. elegans), often used by researchers as a model to investigate lifespan. The researchers discovered an enzyme called VRK-1 works in tandem with AMPK to regulate cellular energy processes.

KAIST 的这项新研究集中在一种微小的蛔虫—- 秀丽隐杆线虫—- 的这一通路上,研究人员经常用它作为研究寿命的模型。研究人员发现一种叫做 VRK-1的酶与 AMPK 一起调节细胞的能量过程。

Boosting VRK-1 activity in the roundworms extended the organism’s lifespan by stimulating AMPK activity, and inhibiting the enzyme reduced its lifespan. Moving to laboratory cell tests the researchers verified this VRK-1 to AMPK mechanism does seem to occur in human cells, suggesting it is possible the lifespan-extending results may be replicated in human subjects.

通过刺激 AMPK 活性,提高蛔虫体内 VRK-1的活性,延长了生物体的寿命,并抑制了这种酶的活性,减少了它的寿命。移动到实验室细胞测试研究人员证实这个 VRK-1到 AMPK 的机制似乎确实发生在人类细胞中,这表明延长寿命的结果有可能在人类受试者中复制。

“This raises the intriguing possibility that VRK-1 also functions as a factor in governing human longevity, and so perhaps we can start developing longevity-promoting drugs that alter the activity of VRK-1,” explains Seung-Jae V. Lee, who lead the new research.

领导这项新研究的李解释说: “这提出了一个耐人寻味的可能性,即 VRK-1也可以作为控制人类寿命的因素,所以也许我们可以开始开发能改变 VRK-1活性的延长寿命的药物。”。

It is still extraordinarily early days for the research, and the next steps will be to explore the effects of modulating VRK-1 activity in more complex animal models such as rodents. Lee says the success in replicating this VRK-1 to AMPK mechanism in human cells suggests the pathway may be relevant in a number of complex organisms, but it is still unclear how this could be harnessed for therapeutic outcomes.

这项研究还处于非常早期的阶段,接下来的步骤将是探索调节 VRK-1活性在更复杂的动物模型中的作用,比如啮齿动物。李说,在人类细胞中成功地将这种 VRK-1复制到 AMPK 机制表明,这种途径可能与许多复杂的生物体有关,但是目前还不清楚如何利用这种途径达到治疗效果。

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