Cigarette Smoking Drives Thyroid Eye Disease Progression via RAGE Signaling Activation
Authors' conclusion
Cigarette smoking-relevant TED progression was linked with RAGE signaling activation, leading to the exacerbation of orbital inflammation and tissue-remodeling, including fibrosis and adipogenesis.
Study context
- Population
- Orbital fibroblasts (OFs) from patients with thyroid eye disease (TED) and non-TED controls; TED mouse model exposed to cigarette smoke
- Comparison
- Cigarette smoking extract (CSE)-treated vs untreated OFs; RAGE blockade vs none
Methodological detailsin vitro orbital fibroblasts, adenovirus-induced TED mouse model
- In vitro orbital fibroblasts
- Adenovirus-induced TED mouse model
Main finding
As reported in the abstract
- CSE exposure caused an inflammatory phenotype of OFs with higher oxidative stress
- CSE-exposed OFs susceptible to TGF-β-induced myofibroblast and 15-D-PGJ2-induced adipocyte differentiation (pro-fibrotic, pro-adipogenic)
- RNA-sequencing of CSE-treated OFs showed upregulated RAGE signaling molecules
- TED patients with smoking history had higher RAGE signaling in orbit and peripheral blood vs non-smoking patients
- Enhanced inflammation associated with ROS-NF-κB pathway activation downstream of RAGE
- RAGE gene interference or RAGE inhibitor mitigated smoking-related pathological changes in OFs
- Disrupting RAGE signaling in TED mice ameliorated smoking-induced disease progression in vivo
Original publication
Cigarette Smoking Drives Thyroid Eye Disease Progression via RAGE Signaling Activation. Thyroid. Published 12 June 2025. doi:10.
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