Elucidating the role of Brain-Derived Neurotrophic Factor (BDNF) and its receptor Tyrosine Receptor Kinase B (TrkB) in the development and symptoms of endometriosis

Endometriosis (EMs) is a common disease among women of reproductive age, and as of now, the clinical understanding of the etiology of this disease remains unclear. The occurrence of EMs has a profound impact on the reproductive health of women, making early diagnosis and treatment of this disease a pressing challenge in clinical practice. Recent studies have found that Brain-Derived Neurotrophic Factor (BDNF), in combination with its high-affinity receptor Tyrosine Receptor Kinase B (TrkB), participates in the development of EMs and the appearance of clinically relevant symptoms by activating the Mitogen-Activated Protein Kinase (MAPK) pathway, the Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) pathway, and the Phospholipase C-gamma (PLCγ) signaling pathway, or by interacting with other factors. In order to gain a deeper understanding of the pathogenesis related to EMs, this article reviews the roles of BDNF and TrkB in EMs, particularly in terms of aberrant apoptosis and autophagy, cell invasion, proliferation, angiogenesis, oxidative stress, and inflammatory reactions, as well as their relationship with the symptoms associated with EMs.