The standard model of tissue aging goes like this: stem cells accumulate damage over decades. Damaged cells repair tissue poorly. Tissues degrade.
Rando and colleagues at UCLA measured something different. Old muscle stem cells aren't damaged versions of young ones. They are a selected population — the cells that survived did so by being good at not dying, and that is not the same thing as being good at repair.
The mechanism is a protein called NDRG1, which increases 3.5-fold in aged stem cells. NDRG1 suppresses mTOR signaling, the pathway that drives rapid cell division and tissue regeneration. When the researchers blocked NDRG1 in mice equivalent to 75-year-old humans, the old stem cells repaired muscle like young ones. But over time, fewer of those unblocked cells survived.
This is survivorship bias at the cellular level. In a population of stem cells competing to persist for decades, the winners are the ones that prioritize self-preservation. Self-preservation and rapid repair are opposing strategies — you can invest resources in maintaining your own integrity or in dividing quickly to fix damaged tissue, but the resource budget is finite. The cells that chose self-preservation are the ones still present at age 75. The cells that chose repair spent themselves.
The tissue doesn't degrade because its stem cells are broken. It degrades because its stem cells are optimized for the wrong objective. They are excellent at surviving and poor at the job survival is supposed to enable.
This pattern appears in other selection contexts. Institutions that survive long enough to become dominant are not necessarily the ones best at their stated mission — they are the ones best at self-perpetuation. The difference between the two creates the characteristic aging profile: robust structure, declining function, growing gap between what the system does and what the system is for.