Mitochondria-Targeting Antibiotics Extend Lifespan in C. Elegans
11-22-2023“Our ultimate goal is to find existing FDA-approved drugs and dietary supplements that can not only increase lifespan but also improve healthspan.”
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BUFFALO, NY- November 22, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Antibiotics that target mitochondria extend lifespan in C. elegans.”
Aging is a continuous degenerative process caused by a progressive decline of cell and tissue functions in an organism. It is induced by the accumulation of damage that affects normal cellular processes, ultimately leading to cell death. It has been speculated for many years that mitochondria play a key role in the aging process.
In this new study, researchers Gloria Bonuccelli, Darren R. Brooks, Sally Shepherd, Federica Sotgia, and Michael P. Lisanti from the University of Salford aimed to characterize the implications of mitochondria in aging using Caenorhabditis elegans (C. elegans) as an organismal model. The C. elegans were treated with a panel of mitochondrial inhibitors and assessed for survival.
“In our study, we assessed survival by evaluating worm lifespan, and we assessed aging markers by evaluating the pharyngeal muscle contraction, the accumulation of lipofuscin pigment and ATP levels.”
Their results show that treatment of worms with either doxycycline, azithromycin (inhibitors of the small and the large mitochondrial ribosomes, respectively), or a combination of both, significantly extended median lifespan of C. elegans, enhanced their pharyngeal pumping rate, reduced their lipofuscin content and their energy consumption (ATP levels), as compared to control untreated worms, suggesting an aging-abrogating effect for these drugs. Similarly, DPI, an inhibitor of mitochondrial complex I and II, was capable of prolonging the median lifespan of treated worms. On the other hand, subjecting worms to vitamin C, a pro-oxidant, failed to extend C. elegans lifespan and upregulated its energy consumption, revealing an increase in ATP level.
“Therefore, our longevity study reveals that mitochondrial inhibitors (i.e., mitochondria-targeting antibiotics) could abrogate aging and extend lifespan in C. elegans.”
Read the full study: DOI: https://doi.org/10.18632/aging.205229
Corresponding Authors: Michael P. Lisanti, Federica Sotgia
Corresponding Emails: m.p.lisanti@salford.ac.uk, f.sotgia@salford.ac.uk
Keywords: C. elegans, aging, lifespan, lipofuscin, antibiotics, mitochondria, metabolism, DPI
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About Aging-US:
Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.
Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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