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Fu Lei’s Team Published Paper in Top Academic Journal PNAS

April 20, 2020      Author: Zhang Yang, Zhang Dongdong, Hu Yixin

Fu Lei's team have finished a staged research on "chemical intervention in mitochondrial activity", and published a paper titled "Moderation of Mitochondrial Respiration Mitigates Metabolic Syndrome of Aging" in the journal PNAS.

A person's health span is the length of time that the person is healthy - not just alive. According to a paper in the April 2020 issue of Proceedings of the National Academy of Sciences of the United States of America (PNAS), scientists from Shanghai Jiao Tong University and Stanford University designed a novel drug, TPP-thiazole, a member of Mito-Fu family. This compound specifically targets mitochondria and consequentially alleviates aging diseases, impedes the onset of age-associated obesity, blood glucose complications, and improves health span in mice.

"We have discovered a proprietary mechanism to improve mitochondrial quality and quantity in the animal model." says Professor Fu at SJTU School of Pharmacy, a corresponding author of this PNAS paper, "these compelling results in mice show that the impact of this compound deserves a closer look as there are many potential clinical applications based on this proprietary mechanism."


The impacts of an added inhibitor on a variety of mitochondrial functions were analyzed, such as respiratory activity, mitochondrial bioenergetics, and biogenesis, and a few age-associated comorbidities, including reactive oxygen species (ROS) production, glucose abnormalities, and obesity in mice. It was found that mitochondrial quality, dynamics, and oxidative metabolism were greatly improved, resulting in lean mice with a specific reduction in visceral fat plus superb energy and glucose homeostasis during their aging period compared to the control group. These results strongly suggest that a mild interference in ATP synthesis through moderation of mitochondrial activity could effectively up-regulate mitogenesis, reduce ROS production, and preserve mitochondrial integrity, thereby impeding the onset of metabolic syndrome. We conclude that this inhibitory intervention in mitochondrial respiration rectified the age-related physiological breakdown in mice by protecting mitochondrial function and markedly mitigated certain undesired primary outcomes of metabolic syndrome, such as obesity and type 2 diabetes. This intervention warrants further research on the treatment of metabolic syndrome of aging in humans.

Paper Link: https://doi.org/10.1073/pnas.1917948117


 Translated  by Li Wenqi     Reviewed by Wang Bingyu