解码衰老关系:揭示延长寿命的基因网络和药理学策略以及甲苏拉悖论

Anamitra Goswami
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引用次数: 0

摘要

我们都想知道--基因和药物是否能延长我们的寿命。根据《圣经》记载,玛土撒拉的寿命长达 969 年。最近的研究发现了玛土撒拉基因,这是一个特定的DNA片段,具有促进健康茁壮成长的潜力。这一发现为开发旨在延长人类寿命的药物干预开辟了新途径。衰老是一个受自然选择影响的复杂过程,随着时间的推移,衰老逐渐适应了细胞衰老和遗传不稳定性等因素。有关衰老的研究广泛采用了无脊椎动物模型,如刺胞动物、蠕虫、苍蝇和酵母。利用这些生物的遗传方法,发现了许多衰老基因。值得注意的是,有令人信服的证据表明,包括哺乳动物在内的不同物种的长寿途径具有进化保护性。在寻找奥米克研究的过程中,我们将考虑在无脊椎动物身上进行的另一组实验数据,并以间接的方式说明 "衰老生物学 "的巨大进步。蛇尾目动物,如 Turritopsis dohrnii,展示了 "本体逆转",即恢复到早期阶段,从而通过繁殖后的反复返老还童实现生物永生。另外,白藜芦醇和雷帕霉素等化合物已被确认具有延缓模式生物衰老的能力。不过,到目前为止,只有雷帕霉素在小鼠实验中显示出对长寿的影响。目前,无论是通过已有的微小分子组,还是通过众多新兴的替代品,都有机会延缓人类衰老。在此背景下,我们探讨了将与衰老相关的研究成果转化为药物的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Decoding the aging nexus: unravelling genetic networks and pharmacological strategies for lifespan extension and the methuselah paradox
We are all interested in knowing- whether genes and drugs can increase our life-span. As per Bible, Methuselah's lifespan lasted for a total of 969 years. Recent research has identified the Methuselah gene, a specific DNA segment that holds the potential to promote robust and healthy aging. This discovery opens new avenues for the development of pharmaceutical interventions aimed at extending human lifespan. Aging, a complex process influenced by natural selection, has evolved over time, adapting to factors such as cellular senescence and genetic instability. Research on aging has extensively employed invertebrate models like cnidarians, worms, flies, and yeast. Utilizing genetic methodologies with these organisms has resulted in the identification of numerous aging genes. Remarkably, there is compelling evidence of evolutionary conservation within longevity pathways across diverse species, including mammals. In search of omic study, we would consider data from another set of experiments performed on Cnidarians and show that there has a great advanced on the `biology of aging’ in an indirect way. Cnidarians, like Turritopsis dohrnii, showcase "ontogeny reversal," reverting to earlier stages, thus achieving biological immortality through repeated rejuvenation after reproduction. Alternatively, compounds like resveratrol and rapamycin, have been identified as having the ability to decelerate aging in model organisms. However, as of now, only rapamycin has demonstrated an impact on longevity in experiments on mice. The opportunity to postpone human aging currently exists, whether through established groups of tiny molecules or numerous emerging alternatives. In this context, we explore the approaches to convert findings from age-related research into pharmaceuticals.
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