TRPM2 Gene Polymorphism, NLRP3 Inflammasome Expression in Vitiligo Patients

Vitiligo is a chronic autoimmune depigmenting disorder characterized by selective loss of melanocytes. Oxidative stress plays a central role in triggering melanocyte damage. Transient Receptor Potential Melastatin 2 (TRPM2) is a calcium-permeable cation channel activated by reactive oxygen species (ROS). Activation of TRPM2 leads to increased intracellular calcium (Ca2+) influx and mitochondrial dysfunction, contributing to melanocyte apoptosis.

The Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is an intracellular multiprotein complex activated by cellular stress signals, including Ca2+ influx, ROS, and mitochondrial injury. NLRP3 activation results in caspase-1 activation and the release of pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), which further contribute to melanocyte destruction.

Evidence suggests an interaction between TRPM2 activation and NLRP3 inflammasome signaling, particularly under oxidative stress conditions. However, this relationship has not been studied in vitiligo patients. This study investigates TRPM2 gene polymorphism, evaluates NLRP3 expression levels, and explores their association with disease presence and severity.

Inclusion criteria

• Adult patients (aged 18 years and older) clinically diagnosed with vitiligo, either newly diagnosed or not on treatment for at least 3 months before the study.

Exclusion criteria

• Any participant with associated inflammatory disease (such as infections or autoimmune disorders).
• Patients with chronic diseases including cardiac, hepatic, hematologic, or renal disorders, or malignancies.
• Patients who had recent major surgical procedures.
• Patients with segmental vitiligo.
• Vitiligo patients who have received treatment within 3 months prior to the study.