Our laboratory focuses on researching the pathogenesis of endometriosis and developing therapeutic strategies for this widespread cause of infertility and agonizing condition affecting women of fertile age worldwide. While endometriosis is highly prevalent, its exact etiology remains speculative, and current treatments aim to alleviate symptoms rather than targeting the root cause. We aim to investigate the impact of hypoxia-induced polarization of macrophages on endometriosis progression and explore the selective targeting of the M2 macrophage population using a proapoptotic m2pep KLA fusion peptide. Our research uniquely examines the endometriosis-macrophage crosstalk under hypoxic conditions in a tightly regulated environment, seeking to uncover critical molecular mechanisms underlying hypoxia-induced M2 activation in endometriotic pathogenesis. Through the use of physiologically relevant mice endometrial stromal cell culture (ESCC) and macrophage culture models, as well as human endometrial stromal cell culture, we aim to decipher the complex interactions involved. Validation of our findings will be conducted using in vivo endometriotic mice models and Human 3D endometrial organoid models. By elucidating the potential of a molecular-targeting approach for M2 macrophage depletion, our research strives to contribute to more effective treatment strategies and ultimately improve the management of endometriosis, addressing the unmet medical need in the field. Collaboration with researchers, clinicians, and institutions is highly encouraged to foster a comprehensive approach to endometriosis research, and the research is supported by grants from various funding agencies dedicated to advancing women's health.
