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editorial
. 2022 Jun 7;2022(3):hoac023. doi: 10.1093/hropen/hoac023

Figure 1.

Figure 1.

Simplified illustration of postulated mechanisms how chronic endometritis (CE) might impact female fertility (modified from Buzzaccarini et al., 2020). Reported pathophysiological effects of CE on immune cells and gene expression. contradictory results (marked by asterisks) were reported for IGFBP-1 (up- and downregulated and BAX (unaffected, respectively upregulated). BAX, Bcl-2-associated X protein; BCL2, B-cell lymphoma 2; CASP8, Caspase-8; CCL, Chemokine (C-C motif) ligands; CXCL, chemokine (C-X-C motif) ligand; EGFR, epidermal growth factor receptor; IGF-1, insulin-like growth factor 1; IGFBP-1, insulin-like growth factor-binding protein 1; IL, interleukin; MΦ, macrophages; LC3, microtubule-associated proteins 1A/1B light chain 3B; LPS, lipopolysaccharides; mTORC1, mTOR Complex 1; O2, superoxide; PC, plasma cells; TIMP-1, TIMP metallopeptidase inhibitor 1; TGF β, transforming growth factor beta; uNK, uterine natural killer cells; Th, T helper cells; TLR, Toll-like receptors.