Not sure if this has been posted before so apologies if it has.
mTORC1 induces plasma membrane depolarization and promotes preosteoblast senescence by regulating the sodium channel Scn1a | Bone Research
So this relates to the fantastic work being done by Michael Levin. I was digging around to see if senescent cells have a different membrane potential to normal cells and of course they do. And in bone cells at least, this is caused by over activity of mTORC1. And we know that rapamycin inhibits mTORC1.
So this leads me to other questions:
Do other types of senescent cells have other dysfunctional ion channels?
Could they be normalised by other drugs?
Is it better to try to normalise senescent cells than to kill them?
And so on.