Abstract
Uterine fibroids, also known as leiomyomas, are benign tumors of the uterus that disproportionately affect women of reproductive age, often leading to significant clinical symptoms such as abnormal bleeding, pelvic pain, and infertility. Although hormones like estrogen and progesterone have long been established as major contributors to fibroid development, recent advances have shed light on the critical role of growth factors in modulating tumor growth and fibrosis. Among these, platelet-derived growth factor (PDGF) has emerged as a key mediator of cellular proliferation, extracellular matrix deposition, and angiogenesis within fibroid tissues. PDGF exists in several isoforms (AA, BB, AB, CC, DD) and signals through PDGF receptors α and β, activating downstream pathways such as PI3K/AKT, RAS/MAPK, and JAK/STAT. These signaling events promote not only smooth muscle cell proliferation but also fibrotic remodeling by stimulating collagen and fibronectin production. PDGF also interacts with other pathways (particularly transforming growth factor-beta and sex hormones) to amplify fibroid growth and resistance to apoptosis, reinforcing a fibrotic, hormone-responsive microenvironment. Elevated expression of PDGF and its receptors in fibroids compared to normal myometrium supports its central role in pathogenesis.