Melasma is a commonly acquired hyperpigmentation disorder characterized by symmetrical facial macules, with a notably higher prevalence in women and individuals with darker skin tones. Its etiology involves a multifactorial interplay of genetic predisposition, ultraviolet radiation exposure, and hormonal factors. This review consolidates current evidence highlighting the instrumental roles of estrogen and progesterone in modulating melanogenesis. These hormones regulate melanocyte activity via genomic and non-genomic signaling pathways, impacting key enzymes and transcription factors critical to pigment synthesis. Furthermore, crosstalk between hormonal signaling cascades exacerbates hyperpigmentation, contributing to the development of melasma. Therapeutically, targeting endocrine pathways is a promising yet investigational approach, as long-term clinical data remain scarce. Interventions such as receptor modulators and metabolic inhibitors may offer potential for reducing melanin production. Elucidating these endocrine mechanisms provides essential insights for developing more effective and personalized therapeutic strategies for melasma.