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作为研究衰老突变的有用模型。

as a Useful Model for Studying Aging Mutations.

机构信息

Department of Endocrinology and Metabolism, First Affiliated Hospital of Jilin University, Changchun, China.

出版信息

Front Endocrinol (Lausanne). 2020 Oct 5;11:554994. doi: 10.3389/fendo.2020.554994. eCollection 2020.

Abstract

The genome possesses homologs of about two-thirds of all human disease genes. Based on its physiological aging characteristics and superiority, the use of as a model system for studies on aging, age-related diseases, mechanisms of longevity, and drug screening has been widely acknowledged in recent decades. Lifespan increasing mutations in were found to delay aging by impinging several signaling pathways and related epigenetic modifications, including the insulin/IGF-1 signaling (IIS), AMP-activated protein kinase (AMPK), and mechanistic target of rapamycin (mTOR) pathways. Interestingly, dietary restriction (DR) has been shown to increase the lifespan of numerous metazoans and protect them from multiple age-related pathologies. However, the underlying molecular mechanisms are unclear. In recent decades, has been used as a unique model system for high-throughput drug screening. Here, we review mutants exhibiting increased in lifespan and age-dependent changes under DR, as well as the utility of for drug screening. Thus, we provide evidence for the use of this model organism in research on the prevention of aging.

摘要

基因组拥有大约三分之二的人类疾病基因的同源物。基于其生理衰老特点和优势,近几十年来,已广泛将其作为衰老、与年龄相关疾病、长寿机制和药物筛选研究的模型系统。研究发现,在 中增加寿命的突变通过影响几种信号通路和相关的表观遗传修饰,包括胰岛素/胰岛素样生长因子-1 信号通路(IIS)、AMP 激活的蛋白激酶(AMPK)和雷帕霉素机制靶蛋白(mTOR)通路,从而延缓衰老。有趣的是,饮食限制(DR)已被证明可以增加许多后生动物的寿命,并保护它们免受多种与年龄相关的病理。然而,其潜在的分子机制尚不清楚。近几十年来, 已被用作高通量药物筛选的独特模型系统。在这里,我们综述了在 DR 下表现出寿命延长和年龄依赖性变化的 突变体,以及 用于药物筛选的效用。因此,我们为该模型生物在衰老预防研究中的应用提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46e4/7570440/a04426f65773/fendo-11-554994-g0001.jpg

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