A narrative review on the role of IL-1β, IL-8, and the endometrial matrix in heavy menstrual bleeding pathogenesis.

Heavy menstrual bleeding (HMB) is a common gynecological condition characterized by excessive menstrual blood loss, often leading to anemia and reduced quality of life. Inflammation plays a crucial role in its pathogenesis, with interleukin-1 beta (IL-1β) and interleukin-8 (IL-8) emerging as key mediators in endometrial dysfunction. IL-1β amplifies inflammatory responses, stimulates matrix metalloproteinases (MMPs), and promotes extracellular matrix (ECM) degradation, leading to increased tissue breakdown and vascular instability. Concurrently, IL-8 recruits neutrophils and drives abnormal angiogenesis, contributing to excessive and prolonged bleeding. The interaction between these cytokines and the ECM disrupts endometrial homeostasis, exacerbating tissue shedding and vascular fragility. IL-1β-induced MMP activation degrades ECM components such as collagen and laminin, weakening the structural integrity of the endometrial lining. Meanwhile, IL-8-mediated neutrophil infiltration and reactive oxygen species release further promote tissue damage. Additionally, IL-8 enhances endothelial cell proliferation, leading to the formation of fragile, easily ruptured blood vessels that exacerbate HMB symptoms.