Fig. 6

Possible relationship between the ANS and endometriosis-associated inflammation endometriotic lesions are formed after retrograde menstruation. Inflammatory cells (neutrophils, macrophages, MCs, and other cells) are recruited to endometriotic lesions, and total nerve fiber density (NFD) is increased. Sympathetic and parasympathetic nerve fiber densities are reduced in endometriotic lesions. Decreased SNF can induce an enhancement of SP-positive nerve fibers and a decreased in CA concentrations. Sema3C, Sema3F, and TNF secreted by macrophages also play vital roles in the reduction in SNF. The binding between ACh and the α-7-nicotinic ACh receptor of macrophages is restrained when the vagal reflex pathway is suppressed, causing an increase in TNF. The three main parts of endometriotic lesions cause the formation and persistence of inflammation, angiogenesis and neurogenesis. Ultimately, most women with endometriosis have various pain symptoms