| First Author | Huang J | Year | 2024 |
| Journal | Int Immunopharmacol | Volume | 127 |
| Pages | 111397 | PubMed ID | 38134596 |
| Mgi Jnum | J:349280 | Mgi Id | MGI:7573938 |
| Doi | 10.1016/j.intimp.2023.111397 | Citation | Huang J, et al. (2023) High mobility group box 1 promotes endometriosis under hypoxia by regulating inflammation and autophagy in vitro and in vivo. Int Immunopharmacol 127:111397 |
| abstractText | BACKGROUND: Endometriosis is a chronic disease. Our previous study identified a positive correlation between high mobility group box 1 (HMGB1) and endometriosis, and HMGB1 and inflammation. However, the precise roles of HMGB1 in endometriosis are not fully elucidated. METHODS: We overexpressed HMGB1 in human endometrial stromal cells (HESCs). The expression of pro-inflammatory cytokines and autophagy-related markers were detected by Western blot and ELISA. We generated HMGB1 deficient mice and established the murine model of endometriosis. The development of endometriosis was evaluated. The expression of cytokines and markers of autophagy in implant lesions and mouse endometrial stromal cells was measured. RESULTS: Overexpression of HMGB1 in HESCs promoted the pro-inflammatory cytokines production and expression of autophagy-related markers. HMGB1 deficient mice had less implant lesions, decreased inflammatory cytokines level and down-regulated autophagy-related markers in implant lesions and mouse endometrial stromal cells. CONCLUSION: HMGB1 promotes endometriosis by regulating inflammation and autophagy. |
