#1

This paper:
https://doi.org/10.1002/advs.202204826
“Exosome release delays senescence by disposing of obsolete bio molecules.”

suggests a pathway/mechanism by which rapamycin extends LS. Namely, by reducing the burden of senescent cells by increasing exosome production and release. The exosomes contain cellular “garbage” which otherwise will eventually accumulate and cause the cell to senesce.
Apologies if already posted by I don’t recall seeing it before.
Cheers
DrT

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#2

Very interesting. Hopefully more research gets done on this.

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#3

Cellular waste, mTOR, autophagy, exosomes, and aging

As we age, our cells accumulate waste. This waste can damage cells and cause them to die, a process called cell senescence.

mTOR is a protein that controls cell growth and metabolism. When mTOR is active, cells grow and divide. When mTOR is inactive, cells break down waste through autophagy, a process of cleaning up cellular waste.

Exosomes are tiny vesicles that cells release to communicate with each other. They can also carry waste products out of cells.

Scientists have discovered that exosomes play a key role in removing cellular waste and delaying aging. Stimulating exosome release by inhibiting mTOR or activating autophagy may be a new way to delay aging and improve health.

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#4

@DrT Great paper. It provides another link between Rapamycin, senescence and longevity.

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#5

Jonas, nice summary.
But a small technical correction needed for your first paragraph. Senescence does not equal cell death. Senescent cells are not dead, but not do they divide. They continue to live, but produce harmful cytokines and molecules.

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#6

Night of the living dead :joy:

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#7

Thanks for the teaching! We are lucky to have some doctors in the house!

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