Reporter brief
Rapamycin reversed cigarette smoke-induced autophagy impairment in rat lung cells and human cell cultures.
What happened
A preclinical study exposed rats to cigarette smoke for 8 weeks and treated human bronchial epithelial cells with cigarette smoke extract to model COPD-related cellular senescence. Rapamycin (an autophagy activator) reversed impaired autophagic flux and cellular senescence markers in both in vivo and in vitro models, while the AhR antagonist CH223191 and ROS scavenger NAC similarly restored autophagy and reduced senescence.
Why it matters
Assessment pending; this report does not establish a change in evidence.
What it does NOT prove
- Limitations have not been recorded; consult the primary source.
Study design and sample
Preclinical; Mixed.
Rats exposed to whole-body cigarette smoke for 8 weeks and human bronchial epithelial BEAS-2B cells treated with cigarette smoke extract
- Design
- Preclinical
- Sample
- —
- Journal
- Tobacco induced diseases
- Published
- Sep 9, 2026
Effect size
Not recorded.
Caveats
- Assessment: Pending.
- Only the source material recorded on this evidence page was assessed.
Conflicts and funding
Not recorded.
Previous evidence
See the Rapamycin timeline and recorded assessment for prior evidence.
Primary source
Cancel Death charts and briefs may be reproduced editorially with attribution to CancelDeath.com. This brief is generated from the primary recorded source facts and assessment. Its review status is shown below; verify quotations against the paper before publication.