Cellular survivorship bias as a mechanistic driver of muscle stem cell aging.

Jengmin Kang, Daniel I Benjamin, Qiqi Guo, Chauncey Evangelista, Soochi Kim, Marina Arjona, Pieter Both, Mingyu Chung, Ananya K Krishnan, Gurkamal Dhaliwal, Richard Lam, Thomas A Rando

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA. · pubmed

Paper

Abstract

Aging is characterized by a decline in the ability of tissue repair and regeneration after injury. In skeletal muscle, this decline is largely driven by impaired function of muscle stem cells (MuSCs) to efficiently contribute to muscle regeneration. We uncovered a cause of this aging-associated dysfunction: a cellular survivorship bias that prioritizes stem cell persistence at the expense of functionality. With age, MuSCs increased expression of a tumor suppressor, N-myc down-regulated gene 1 (NDRG1), which, by suppressing the mammalian target of rapamycin (mTOR) pathway, increased their long-term survival potential but at the cost of their ability to promptly activate and contribute to muscle regeneration. This delayed muscle regeneration with age may result from a trade-off that favors long-term stem cell survival over immediate regenerative capacity.

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Research summary

The paper claims that increased expression of NDRG1 in aging muscle stem cells leads to a trade-off between long-term survival and immediate regenerative capacity. This research is relevant as it addresses a mechanistic driver of muscle stem cell aging, which is a fundamental aspect of the aging process and tissue regeneration.

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