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Biochim Biophys Acta Mol Basis Dis ; 1869(7): 166761, 2023 10.
Artículo en Inglés | MEDLINE | ID: mdl-37247698

RESUMEN

Endometriosis is an estrogen-dependent, progesterone-resistant gynecological disease with an unknown pathogenesis. Compared to women without endometriosis, women with endometriosis have a remarkably high heme level in the peritoneal fluid. To further investigate the pathomechanisms of heme in endometriosis, we aimed to identify the dysregulated expression of heme-trafficking proteins, such as PGRMC1/2 that are also receptors that mediate the non-genomic responses to progesterone, and heme-degrading enzymes between ectopic endometrial stromal cells and their normal counterparts. We found that heme could regulate progesterone receptor-related gene expression. Functional human endometrial stromal cell experiments showed that heme promotes cell proliferation and migration in a heme oxygenase-1-independent manner; moreover, blocking oxidative phosphorylation/ATP generation could abolish these effects of heme in vitro, whereas intraperitoneal hemopexin administration could alleviate heme-triggered ectopic lesions in vivo. Therefore, heme likely mediates the induction of progesterone resistance and simultaneously induces endometriosis via the mitochondrial oxidative phosphorylation pathway.


Asunto(s)
Endometriosis , Enfermedades Uterinas , Femenino , Humanos , Progesterona/farmacología , Progesterona/metabolismo , Endometriosis/genética , Enfermedades Uterinas/metabolismo , Enfermedades Uterinas/patología , Endometrio/patología , Estrógenos/metabolismo , Proteínas de la Membrana/metabolismo , Receptores de Progesterona/genética , Receptores de Progesterona/metabolismo
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