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Updated: Jan 29, 2026
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Author Spotlight: Advancing Allergic Rhinitis Research with Multicolor Immunofluorescence
Published on: September 22, 2023
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Oxidative Stress and PRKN-Mediated Senescence Link RhoA/ROCK Signaling to Epithelial Remodeling in Allergic Rhinitis.
Xuan Yuan1,2, Wei Zhong2, Shaobing Xie1,2
1Division of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Antioxidants (Basel, Switzerland)
|January 28, 2026
Summary
RhoA-driven epithelial senescence exacerbates allergic rhinitis (AR) inflammation and remodeling. Targeting parkin (PRKN) may restore epithelial homeostasis in AR patients.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Allergic rhinitis (AR) involves persistent epithelial remodeling, but underlying mechanisms are unclear.
- Nasal mucosa in AR patients shows remodeling, oxidative stress, and Th2 inflammation.
- RhoA gene expression correlates with AR severity.
Purpose of the Study:
- Investigate the role of RhoA in AR pathogenesis.
- Determine the link between RhoA, cellular senescence, and AR.
- Identify therapeutic targets for AR.
Main Methods:
- Analysis of nasal mucosa from AR patients.
- Epithelial-specific RhoA-deficient mice (RhoA^cKO) and RhoA/ROCK inhibitor (fasudil).
- Transcriptome analysis, in vitro and in vivo cellular senescence studies, and PRKN functional studies.
Main Results:
- Loss of RhoA/ROCK signaling reduced Th2 inflammation, oxidative stress, and remodeling in mice.
- RhoA activation promoted epithelial cellular senescence.
- Eliminating senescent cells alleviated AR inflammation and remodeling.
- PRKN overexpression mitigated IL-13-induced mitochondrial dysfunction and senescence.
Conclusions:
- RhoA-driven epithelial senescence contributes to allergic inflammation and remodeling in AR.
- PRKN is a potential therapeutic target for restoring epithelial homeostasis in AR.
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