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鲍鱼肽通过 SKN-1 调控的转录代谢重编程增加秀丽隐杆线虫的应激弹性和无成本寿命。

Abalone peptide increases stress resilience and cost-free longevity via SKN-1-governed transcriptional metabolic reprogramming in C. elegans.

机构信息

Institute for Food Nutrition and Human Health, School of Food Science and Engineering, South China University of Technology, Guangzhou, China.

Guangdong Province Key Laboratory for Biocosmetics, Guangzhou, China.

出版信息

Aging Cell. 2024 Feb;23(2):e14046. doi: 10.1111/acel.14046. Epub 2023 Nov 22.

Abstract

A major goal of healthy aging is to prevent declining resilience and increasing frailty, which are associated with many chronic diseases and deterioration of stress response. Here, we propose a loss-or-gain survival model, represented by the ratio of cumulative stress span to life span, to quantify stress resilience at organismal level. As a proof of concept, this is demonstrated by reduced survival resilience in Caenorhabditis elegans exposed to exogenous oxidative stress induced by paraquat or with endogenous proteotoxic stress caused by polyglutamine or amyloid-β aggregation. Based on this, we reveal that a hidden peptide ("cryptide")-AbaPep#07 (SETYELRK)-derived from abalone hemocyanin not only enhances survival resilience against paraquat-induced oxidative stress but also rescues proteotoxicity-mediated behavioral deficits in C. elegans, indicating its capacity against stress and neurodegeneration. Interestingly, AbaPep#07 is also found to increase cost-free longevity and age-related physical fitness in nematodes. We then demonstrate that AbaPep#07 can promote nuclear localization of SKN-1/Nrf, but not DAF-16/FOXO, transcription factor. In contrast to its effects in wild-type nematodes, AbaPep#07 cannot increase oxidative stress survival and physical motility in loss-of-function skn-1 mutant, suggesting an SKN-1/Nrf-dependent fashion of these effects. Further investigation reveals that AbaPep#07 can induce transcriptional activation of immune defense, lipid metabolism, and metabolic detoxification pathways, including many SKN-1/Nrf target genes. Together, our findings demonstrate that AbaPep#07 is able to boost stress resilience and reduce behavioral frailty via SKN-1/Nrf-governed transcriptional reprogramming, and provide an insight into the health-promoting potential of antioxidant cryptides as geroprotectors in aging and associated conditions.

摘要

健康老龄化的一个主要目标是预防弹性下降和脆弱性增加,这与许多慢性疾病和应激反应恶化有关。在这里,我们提出了一个损失或获得生存模型,用累积应激跨度与寿命的比值来量化机体水平的应激弹性。作为一个概念验证,这在秀丽隐杆线虫暴露于百草枯引起的外源性氧化应激或聚谷氨酰胺或淀粉样β聚集引起的内源性蛋白毒性应激时,生存弹性降低得到了证明。基于这一点,我们揭示了一种隐藏的肽(“隐肽”)-来自鲍鱼血蓝蛋白的 AbaPep#07(SETYELRK)-不仅增强了对百草枯诱导的氧化应激的生存弹性,而且挽救了秀丽隐杆线虫中蛋白毒性介导的行为缺陷,表明其具有抵抗应激和神经退行性变的能力。有趣的是,AbaPep#07 还被发现可以增加线虫的无成本寿命和与年龄相关的身体适应性。然后,我们证明 AbaPep#07 可以促进 SKN-1/Nrf 的核定位,而不是 DAF-16/FOXO 转录因子。与在野生型线虫中的作用相反,AbaPep#07 不能增加 skn-1 突变体的氧化应激生存和身体运动能力,表明这些作用是 SKN-1/Nrf 依赖的方式。进一步的研究表明,AbaPep#07 可以诱导免疫防御、脂质代谢和代谢解毒途径的转录激活,包括许多 SKN-1/Nrf 靶基因。总之,我们的研究结果表明,AbaPep#07 通过 SKN-1/Nrf 调控的转录重编程能够提高应激弹性,减少行为脆弱性,并为抗氧化隐肽作为衰老和相关疾病的抗衰老保护剂的促进健康潜力提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e950/10861207/0a8e96431f48/ACEL-23-e14046-g002.jpg

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