Caenorhabditis elegans as a Useful Model for Studying Aging Mutations

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...

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Published inFrontiers in endocrinology (Lausanne) Vol. 11; p. 554994
Main Authors Zhang, Siwen, Li, Fei, Zhou, Tong, Wang, Guixia, Li, Zhuo
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 05.10.2020
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Summary: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.
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Edited by: Alessandro Cellerino, Normal School of Pisa, Italy
Reviewed by: Collin Ewald, ETH Zürich, Switzerland; Patrizia D'Aquila, University of Calabria, Italy
This article was submitted to Endocrinology of Aging, a section of the journal Frontiers in Endocrinology
ISSN:1664-2392
1664-2392
DOI:10.3389/fendo.2020.554994