Rapamycin reversed cigarette smoke-induced autophagy impairment in rat lung cells and human cell cultures.
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.
What this changes
The finding has not established an approved change to our evidence assessment.
Source date: Sep 9, 2026 · Discovered: Sep 16, 2026 · Assessed: — · Research update
What it does not prove
- Limitations have not yet been verified. Read the primary source.
Extracted from supplied source material; model confidence is not a measured probability of correctness.
Study details
- Design
- Preclinical
- Sample size
- —
- Duration
- 2 months
- Population
- Rats exposed to whole-body cigarette smoke for 8 weeks and human bronchial epithelial BEAS-2B cells treated with cigarette smoke extract
- Primary outcome
- Cellular senescence in lung tissue and epithelial cells
- Effect size
- —
- Significance
- Significant
- Journal
- Tobacco induced diseases
- Published
- Sep 9, 2026
Sources
Primary source
- Tobacco induced diseases ↗Peer reviewed
Assessment history
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