However, therapies targeting these molecules have shown contradictory results, underscoring the need for further research to find effective treatments.2527 Autoimmunity Genetic evidence supports the autoimmune hypothesis as the main mechanism of vitiligo, with approximately 85% of susceptibility genes involved in innate, adaptive immunity, and apoptosis.4,28 This theory is also reinforced by the relationship of vitiligo with other autoimmune disorders, the presence of specific antibodies in patients, and the use of immunomodulatory therapies.4,28 Furthermore, it has been observed that treatments with immune checkpoint inhibitors in cancer patients can induce the development of vitiligo, suggesting a link between autoimmunity and this disease.29 Autoimmune diseases are the main comorbidity associated with vitiligo, including thyroid disorders, pernicious anemia, alopecia areata, connective tissue diseases, among others.30,31 Zombie cells, senescent cells in vitiligo Cellular senescence is induced in response to cellular stressors
Molecules (2014)
Oxidative stress can induce the expression of the p53 gene during epileptic seizures (Tong et al
12 mg subcutaneous daily , or 1 mg three times weekly , is the most commonly used GHK-Cu skin dose in published research and clinic practice
