The pathogenesis of OHSS. Human chorionic gonadotropin (hCG) stimulates a high number of granulosa-lutein cells leading to the increased production of vascular endothelial growth factor (VEGF) mRNA (Figure 1A); VEGF receptor-2 (VEGFR-2) mRNA production in the granulosa-lutein and endothelial cells is also increased in response to hCG. High amounts of VEGF are produced and released from the granulosa-lutein cells and bind to VEGFR-2 on the endothelial cell membranes. Downstream signaling augments vascular permeability (Figure 1B). Adapted from Soares et al .