作者
Parminder Singh,Kishore Gollapalli,Stefano Mangiola,Daniela Schranner,Mohd Aslam Yusuf,Manish Chamoli,Sting L. Shi,Bruno Lopes-Bastos,Tripti Nair,Annett Riermeier,Elena Vayndorf,Judy Wu,Aishwarya Nilakhe,Christina Q. Nguyen,Michael Muir,Michael G. Kiflezghi,Anna Foulger,Alex Junker,Jack Devine,Kunal Sharan,Shankar J. Chinta,Swati Rajput,Anand Rane,Philipp Baumert,Martin Schönfelder,Francescopaolo Iavarone,Giorgia Di Lorenzo,Swati Kumari,Alka Gupta,Rajesh Sarkar,Costerwell Khyriem,Amanpreet Singh Chawla,Ankur Sharma,Nazan Sarper,Naibedya Chattopadhyay,B.K. Biswal,Carmine Settembre,Perumal Nagarajan,Kimara L. Targoff,Martin Picard,Sarika Gupta,Vidya Velagapudi,Anthony T. Papenfuss,Alaattin Kaya,Miguel Godinho Ferreira,Brian K. Kennedy,Julie K. Andersen,Gordon J. Lithgow,Abdullah Mahmood Ali,Arnab Mukhopadhyay,Aarno Palotie,Gabi Kastenmüller,Matt Kaeberlein,Henning Wackerhage,Bhupinder Pal,Vijay K. Yadav
摘要
Aging is associated with changes in circulating levels of various molecules, some of which remain undefined. We find that concentrations of circulating taurine decline with aging in mice, monkeys, and humans. A reversal of this decline through taurine supplementation increased the health span (the period of healthy living) and life span in mice and health span in monkeys. Mechanistically, taurine reduced cellular senescence, protected against telomerase deficiency, suppressed mitochondrial dysfunction, decreased DNA damage, and attenuated inflammaging. In humans, lower taurine concentrations correlated with several age-related diseases and taurine concentrations increased after acute endurance exercise. Thus, taurine deficiency may be a driver of aging because its reversal increases health span in worms, rodents, and primates and life span in worms and rodents. Clinical trials in humans seem warranted to test whether taurine deficiency might drive aging in humans.