Age-associated decline of Coenzyme A leads to intestinal stem cells dysfunction via disturbing iron homeostasis.

Zhiming Liu, Gang Du, Yi Chen, Haiyang Chen

West China Centre of Excellence for Pancreatitis, and Laboratory of Metabolism and Aging, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Respiratory Health and Multimorbidity and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China. · pubmed

Paper

Abstract

The decline in adult stem cell performance is closely linked to tissue malfunction and the rising incidence of age-related diseases. To investigate the molecular basis of these impairments, our screening strategy identified reduced activity in the pantothenate/coenzyme A (CoA) pathway within aged ISCs. Furthermore, exogenous CoA supplementation restructured ISC metabolic pathways, reversing age-induced hyperproliferation and intestinal dysfunction, and thus extending Drosophila lifespan by curbing excessive iron accumulation in ISCs. These findings uncover a new mechanism of stem cell aging and propose that pantothenate and CoA could be potential therapeutic targets for treating age-related diseases and enhancing healthy aging in humans.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that age-associated decline of Coenzyme A leads to intestinal stem cell dysfunction, which can be reversed by CoA supplementation. This research is relevant as it investigates a potential root cause of aging-related decline in stem cell function and proposes a therapeutic target for enhancing healthy aging.

Author of this paper? Send a correction.