CHIP induces ubiquitination and degradation of HMGB1 to regulate glycolysis in ovarian endometriosis.
Ovarian endometriosis is a common gynecological condition that can cause infertility in women of childbearing age. However, the pathogenesis is still unknown. We demonstrate that the carboxyl terminus of Hsc70-interacting protein (CHIP) is a negative regulator in the development of endometriosis and reduces HMGB1 expression in endometriotic cells. Meanwhile, CHIP ... interacts with HMGB1 and promotes its ubiquitinated degradation, thereby inhibiting aerobic glycolysis and the progression of endometriosis. Furthermore, the CHIP agonist YL-109 effectively suppresses the growth of ectopic endometrium in endometriosis mouse model, which could be a potential therapeutic approach for endometriosis. In conclusion, our data suggest that CHIP may inhibit the development of endometriosis by suppressing the HMGB1-related glycolysis.
Mesh Terms:
Animals, Endometriosis, Female, Glycolysis, HMGB1 Protein, Humans, Mice, Ubiquitin-Protein Ligases, Ubiquitination
Animals, Endometriosis, Female, Glycolysis, HMGB1 Protein, Humans, Mice, Ubiquitin-Protein Ligases, Ubiquitination
Cell Mol Life Sci
Date: Dec. 19, 2022
PubMed ID: 36536161
View in: Pubmed Google Scholar
Download Curated Data For This Publication
245464
Switch View:
- Interactions 4