Fatemeh Kiaee, Heshmat Shahi
Endometriosis is a complex chronic condition, driven by estrogen, characterized by the growth of endometrial-like tissue outside the uterus. This often-debilitating disease affects millions of women globally, manifesting as severe pelvic pain, significant subfertility, and a profound reduction in the quality of their lives. These clinical problems need advancements in both diagnostic tools and therapeutic strategies. This article delves into the intricate relationship between endometriosis-derived lactic acid and a specific subset of immune cells, known as myeloid-derived suppressor cells (MDSCs). We aim to elucidate the nuanced biological pathways that affect this significant interaction. Lactates subsequently drive the expansion and activation of MDSCs, which then increase immune suppression through key signaling molecules such as hypoxia-inducible factor 1-alpha, signal transducer and activator of transcription 3, and nuclear factor kappa-light-chain-enhancer of activated B cells. Beyond its role in immune modulation, this complex interplay between lactic acid and MDSCs is emerging as a pivotal factor in the multifaceted pathogenesis of endometriosis. It significantly contributes to the disease's bad progression, including its invasive spread, the development of new blood vessels (angiogenesis), and the characteristic formation of fibrotic, scar-like tissue. This review hypothesizes that targeted modulation of lactate metabolism could serve as a promising therapeutic strategy to regulate MDSC activity. The purpose of this study is to clarify these intricate cellular and molecular events.