Assessment of the Prognostic Value of SMAD2 Gene Expression in Patients with Otosclerosis
Otosclerosis is a prevalent etiology of auditory impairment which is marked by atypical osseous proliferation in the otic capsule resulting in stapes immobilization. Till now the etiology of the disease is not fully understood , however multifactors are thought to trigger the disease and accelerate its course. The genetic component is extensively researched in the hope of decelerating illness progression or discovering a substantial treatment for affected people. Aim of the study; The objective of the current study is to detect SMAD2 expression as a prognostic biomarker for otosclerosis. Patients and methods; 20 control and 40 otosclerosis patients participated in this study. Patients with mild, moderate and severe degrees of otosclerosis were categorized. The participants were adults, males and females, and had clinically diagnosed otosclerosis with hearing loss, tinnitus, or vertigo. Blood samples were collected, centrifuged, and analyzed using total and microRNA extraction and quantitative real-time PCR. The study used the 2-ΔΔCT method and normalized data to internal control GAPDH. Main findings: SMAD2 gene expression was considerably elevated in patients with otosclerosis compared to the control group, with the highest levels observed in severe cases. Expression levels differed significantly between mild, moderate and severe groups (p value <0.01). Principal conclusion: The findings indicated a substantial correlation between SMAD2 gene expression levels and severity of otosclerosis, suggesting its potential role as a predictive biomarker for the disease.
Authors
- Wael F. Sedik
- Ahlam Mohamed Abdallah
- Samar Muhammad Hemeda Abdelaleem
- Samar Hisham Elsayed
- Reham Gamal
Institutions
- Minia University (EG)
Publication Details
- Journal
- Minia Journal of Medical Research
- Published
- 2025-12-26
- DOI
- https://doi.org/10.21608/mjmr.2025.443520.2144
- Primary Topic
- Ear Surgery and Otitis Media
- Type
- article
- Field-Weighted Citation Impact
- 0.00