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Chop Deficiency Exacerbates Cyclophosphamide-Induced Overactive Bladder via Impaired Macrophage Apoptosis
Ya-Nan Wang1, Xiang-Dong Guo1, Chun-Yu Zhang1
1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Current Medical Science
|July 29, 2025
Summary
C/EBP homologous protein (CHOP) deficiency worsens overactive bladder by increasing inflammation and apoptosis. CHOP inhibition alleviates endoplasmic reticulum stress, suggesting a therapeutic target for overactive bladder.
Area of Science:
- Urology
- Cell Biology
- Molecular Biology
Background:
- Overactive bladder (OAB) significantly impairs quality of life.
- Urinary urgency, frequency, and nocturia characterize OAB.
- The underlying mechanisms of OAB require further elucidation.
Purpose of the Study:
- To investigate the role of C/EBP homologous protein (CHOP) in overactive bladder.
- To explore the mechanism by which CHOP influences OAB pathogenesis.
Main Methods:
- Established OAB mouse models using cyclophosphamide in wild-type and Chop-deficient mice.
- Utilized in vitro models with IL-6-induced bladder epithelial cells.
- Assessed tissue damage, inflammatory cytokines, protein expression (ER stress markers, apoptosis factors), and apoptosis via HE staining, ELISA, Western blot, TUNEL, and flow cytometry.
Main Results:
- CHOP levels were decreased in OAB tissues with increased macrophage infiltration.
- Chop deficiency exacerbated OAB symptoms, tissue injury, macrophage infiltration, and bladder epithelial apoptosis.
- Knockout of Chop alleviated endoplasmic reticulum stress.
Conclusions:
- CHOP deficiency exacerbates inflammation, injury, and apoptosis in OAB model mice.
- This exacerbation occurs by inhibiting endoplasmic reticulum stress.
- CHOP plays a critical role in OAB pathogenesis, potentially via ER stress modulation.
