Only a handful of tissues are believed to be non-renewing in humans—e.g. eggs, neurons, and the lens of the eye
Wikipedia says: Un-repaired DNA damages accumulate in non-replicating cells, such as cells in the brains or muscles of adult mammals, and can cause aging.
Weakening of muscles seems to me like a plausible driver of aging.
Yeah, lots of sources say that various aging-related things “accumulate”. If you dig into it, it turns out that by “accumulate” they usually mean “increases”—DNA damage does not actually stick around for long, it turns over very quickly (see e.g. here, or compare the damage frequencies to the steady state levels on the wikipedia page). But the steady-state level of DNA damage does increase with age (even in many types of replicating cells), so either the damage rate increases or the repair rate decreases.
Weakening of muscles is an interesting case. Muscle “cells” (myocytes) are really huge, centimeter-long super-cells containing hundreds of nuclei, and satellite cells (the first type of stem cell discovered) spin off new nuclei to add to the myocyte on an as-needed basis. So although the cell itself is technically long-lived, that doesn’t mean the components—even including the DNA—aren’t replaced. Loss of muscle mass (sarcopenia) is considered one of the main hallmarks of aging, but as far as I can tell, the gears of sarcopenia are still quite poorly understood. (A lot of people spent a lot of time and effort imaging neuromuscular junctions, but that seems to have been driven more by the desire to publish pretty pictures than by any actual evidence that NMJs play a causal role in sarcopenia.)
Wikipedia says: Un-repaired DNA damages accumulate in non-replicating cells, such as cells in the brains or muscles of adult mammals, and can cause aging.
Weakening of muscles seems to me like a plausible driver of aging.
Yeah, lots of sources say that various aging-related things “accumulate”. If you dig into it, it turns out that by “accumulate” they usually mean “increases”—DNA damage does not actually stick around for long, it turns over very quickly (see e.g. here, or compare the damage frequencies to the steady state levels on the wikipedia page). But the steady-state level of DNA damage does increase with age (even in many types of replicating cells), so either the damage rate increases or the repair rate decreases.
Weakening of muscles is an interesting case. Muscle “cells” (myocytes) are really huge, centimeter-long super-cells containing hundreds of nuclei, and satellite cells (the first type of stem cell discovered) spin off new nuclei to add to the myocyte on an as-needed basis. So although the cell itself is technically long-lived, that doesn’t mean the components—even including the DNA—aren’t replaced. Loss of muscle mass (sarcopenia) is considered one of the main hallmarks of aging, but as far as I can tell, the gears of sarcopenia are still quite poorly understood. (A lot of people spent a lot of time and effort imaging neuromuscular junctions, but that seems to have been driven more by the desire to publish pretty pictures than by any actual evidence that NMJs play a causal role in sarcopenia.)