The role of prolactin аnd dopamine in the pathogenesis of endometriosis
This review analyzes literature on prolactin and dopamine's role in endometriosis pathogenesis and the potential therapeutic use of dopamine agonists.
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This paper reviews the roles of prolactin and dopamine in reproductive physiology and explains how dysregulation of the prolactin axis could contribute to endometriosis pathogenesis, drawing on mechanistic literature about prolactin secretion, dopamine D1/D2 receptor effects, and factors that stimulate or inhibit prolactin. It describes dopamine’s inhibitory control of tuberoinfundibular prolactin release, outlines prolactin biology and receptor distribution, and summarizes how hyperprolactinemia can disrupt luteal function through impaired progesterone production and inhibited GnRH signaling. The authors explicitly note that endometriosis-related prolactin elevation may be multifactorial—linked to hyperestrogenemia, immune activation by ectopic endometrial cells, and pain-associated central neurotransmitter changes—while also referencing that luteal-phase endometrium and potentially endometriotic lesions may secrete prolactin. This paper is centrally about endometriosis — it focuses on prolactin and dopamine pathways as contributors to endometriosis pathogenesis, including proposed mechanisms involving luteal-phase disruption.
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