To elucidate the molecular mechanisms by which oxidative stress contributes to tinnitus and identify potential therapeutic targets, emphasizing the significance of this understanding.
Key Findings:
ACADVL identified as a primary candidate target for tinnitus, with implications for therapeutic strategies.
Increased ACADVL mRNA expression and VLCAD protein levels in tinnitus patients compared to healthy controls.
ACADVL increases tinnitus risk by suppressing CD25 on IgD+CD38− B cells and altering metabolic ratios.
Fenretinide identified as a potential therapeutic agent through molecular docking.
Interpretation:
Oxidative stress-related genes, particularly ACADVL, may increase susceptibility to tinnitus through specific metabolic and inflammatory dysregulation mechanisms.
Limitations:
Limited access to human brain tissue may restrict functional interpretation of genetic findings, and potential biases in study design should be considered.
Most evidence derived from animal models rather than direct human studies.
Conclusion:
This study establishes a framework for investigating the mechanisms of tinnitus and highlights fenretinide as a promising therapeutic candidate, with implications for future treatment strategies.
