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Rapamycin exerts its geroprotective effects in the ageing human immune system by enhancing resilience against DNA damage

Abstract:

mTOR inhibitors such as rapamycin are among the most robust life-extending interventions known, yet the mechanisms underlying their geroprotective effects in humans remain incompletely understood. At non-immunosuppressive doses, these drugs are senomorphic, i.e. they mitigate cellular senescence, but whether they protect genome stability itself has been unclear. Given that DNA damage is a major driver of immune ageing, and immune decline accelerates whole-organism ageing, we tested whether mTOR inhibition enhances genome stability. In human T cells exposed to acute genotoxic stress, we found that rapamycin and other mTOR inhibitors suppressed senescence not by slowing protein synthesis, halting cell division, or stimulating autophagy, but by directly reducing DNA lesional burden and improving cell survival. Ex-vivo analysis of aged immune cells from healthy donors revealed a stark enrichment of markers for DNA damage, senescence, and mTORC hyperactivation, suggesting that human immune ageing may be amenable to intervention by low-dose mTOR inhibition. To test this in vivo, we conducted a placebo-controlled experimental medicine trial in older adults administered with low-dose rapamycin. p21, a marker of DNA damage-induced senescence, was significantly reduced in immune cells from the rapamycin compared to placebo group. These findings reveal a previously unrecognised role for mTOR inhibition: direct genoprotection. This mechanism may help explain rapamycin’s exceptional geroprotective profile and opens new avenues for its use in contexts where genome instability drives pathology, ranging from healthy ageing, clinical radiation exposure, and even the hazards of cosmic radiation in space travel.

 
Publication status:
Published
Peer review status:
Not peer reviewed

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Preprint server copy:
10.1101/2025.08.15.670559

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Botnar Institute for Musculoskeletal Sciences
Research group:
Department of Biochemistry
Oxford college:
Oriel College
Role:
Author
ORCID:
0000-0003-1322-2027
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
NDM Experimental Medicine
Role:
Author
ORCID:
0000-0002-4650-244X


More from this funder
Funder identifier:
https://ror.org/02jkpm469
Grant:
22617


Preprint server:
bioRxiv
Publication date:
2025-08-19
DOI:
EISSN:
2692-8205


Language:
English
Pubs id:
2284071
Local pid:
pubs:2284071
Deposit date:
2025-09-01
ARK identifier:

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