"As muscles age, their stem cells build up high levels of a protein that makes them slower to switch on and repair damaged tissue. At the same time, that same protein helps the cells survive longer in the more stressful environment of older muscle."
"It's counterintuitive, but the stem cells that make it through aging may actually be the least functional ones. They survive not because they're the best at their job, but because they're the best at surviving. That gives us a completely different lens for understanding why tissues decline with age."
"NDRG1 acts like a brake inside the cell. It dampens a signaling pathway known as mTOR, which normally drives cells to activate, grow, and repair tissue."
UCLA researchers discovered that aging muscle stem cells accumulate high levels of NDRG1 protein, which slows their ability to repair damaged tissue by dampening the mTOR signaling pathway. This protein reaches 3.5 times higher levels in older cells compared to younger ones. While NDRG1 reduces repair speed, it simultaneously enhances cell survival in the stressful environment of aging muscle. Removing NDRG1 restores youthful repair capacity but risks depleting the stem cell pool through exhaustion. This finding suggests aging-related biological changes may represent survival strategies rather than simple functional decline, offering a new perspective on tissue aging and regeneration.
Read at ScienceDaily
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