A Nucleic Acid Prodrug That Activates Mitochondrial Respiration, Promotes Stress Resilience, and Prolongs Lifespan.

Takahisa Anada, Michiharu Kawahara, Taisei Shimada, Ryotaro Kuroda, Hidenori Okamura, Daiki Setoyama, Fumi Nagatsugi, Yuya Kunisaki, Eriko Kage-Nakadai, Shingo Kobayashi, Masaru Tanaka

Institute for Materials Chemistry and Engineering, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan.Institute for Materials Chemistry and Engineering, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan. · pubmed

Paper

Abstract

Mitochondrial dysfunction caused by aging leads to decreased energy metabolism, resulting in functional decline and increased frailty in multiple tissues. Strategies for protecting and activating mitochondria under stressful conditions are required to suppress aging and age-related diseases. However, it is challenging to develop drugs capable of boosting mitochondrial respiration and compensating for the reduced intracellular adenosine triphosphate (ATP) levels. In this study, we developed a prodrug that stimulates the metabolism of intracellular adenine nucleotides (AXP: adenosine monophosphate (AMP), adenosine diphosphate (ADP), and ATP). It enhances AMP-activated protein kinase activity, fatty acid oxidation, oxidative stress resistance, and mitochondrial respiration, thereby increasing the intracellular ATP levels. Furthermore, this prodrug markedly extended the lifespan of

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Research summary

The paper claims that a nucleic acid prodrug can enhance mitochondrial respiration and prolong lifespan. This research addresses mitochondrial dysfunction, a root cause of aging, and proposes a novel approach to potentially extend lifespan and improve resilience against age-related decline.

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