Figure 6. Schematic representation of proposed key molecular processes contributing to lesion development. This diagram illustrates the complex interplay between the complement system, coagulation cascade, extracellular matrix remodeling, and immune signaling pathways in the context of lesion formation. Coagulation factors cleave and activate complement components C3 and C5, initiating pro-inflammatory responses. Complement factor C3 also functions to stabilize clots by protecting them from fibrinolysis. The coagulation cascade is tightly regulated by members of the serpin superfamily, which modulate extracellular matrix remodeling through the induction of matrix metalloproteinase-9 (MMP-9) expression. Complement activation further engages the JAK/STAT signaling pathway, particularly STAT5, promoting mast cell activation. Activated mast cells, in turn, influence coagulation dynamics. Pharmacologic inhibition of the JAK/STAT pathway using JAK inhibitors can suppress STAT3 signaling and reduce mast cell degranulation, thereby modulating both inflammatory and thrombotic processes. These mechanisms highlight the therapeutic potential of JAK inhibitors in the context of endometriosis. Genes names in green signify differentially expressed genes, arrows show the directional change in gene expression in endometriosis lesions compared with control endometrium.
Complement and coagulation cascade cross-talk in endometriosis and the potential of Janus Kinase inhibitors—a network meta-analysis #STAT3 #MMP9 #C3 #MECFS #LongCovid
www.frontiersin.org/journals/imm...