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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Autonomic nervous system and inflammation interaction in endometriosis-associated pain

Fig. 3

Inflammation-associated mediators in endometriosis abnormal secretion of inflammation-associated mediators can be found in endometriotic lesions. Increased TGF-β1 promotes the activation and expression of RHOGTPases and induces Aα2-6-sialylation through TGF-βRI-SMAD2/3 signaling. TGF-β1 can also activate the P38MAPK molecular target to pro-inflammatory cytokines. IL-1β stimulates the production of BDNF through JNK, NF-κB, and mechanistic target of rapamycin signal transduction pathways. IL-27 promotes IL-10 production in Th17 cells by c-Maf/RORyt/Blimp-1 signaling. IL-25 and IL-17α enhance the secretion of Gro-α to recruit more neutrophils. PGs can also activate NF-κB to promote the expression of inflammation-related genes, and then, more inflammatory cells are recruited (such as neutrophils and macrophages) and stimulate further cytokine release. In addition, NGF, TNF-α, and other inflammation-associated mediators are increased in endometriotic lesions, resulting in the formation of inflammation and angiogenesis and leading to pain feelings in women with endometriosis

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