ArticleReproductive sciences (Thousand Oaks, Calif.)2021
Estrogen Regulates Endoplasmic Reticulum Stress-Mediated Apoptosis by ERK-p65 Pathway to Promote Endometrial Angiogenesis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- HFTMSCs alleviate uterine fibrosis and restore fertility in intrauterine adhesion models.Reproductive biology and endocrinology : RB&E · 2026Article
- Screening of key active ingredients of Fuyuan Shenghua granules for the treatment of medical abortion using ingredient-target interaction and pharmacokinetics.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Endometrial Aging and Reproductive Decline: The Central Role of Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- Cigarette Smoke Contributes to the Progression of MASLD: From the Molecular Mechanisms to Therapy.Cells · 2025Review
- Review
- The Effect of Granulocyte Colony-Stimulating Factor on Endometrial Receptivity of Implantation Failure Mouse.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- P65 mediated UBR4 in exosomes derived from menstrual blood stromal cells to reduce endometrial fibrosis by regulating YAP Ubiquitination.Journal of nanobiotechnology · 2023Article
- Erbu Zhuyu decoction improves endometrial angiogenesis via uterine natural killer cells and the PI3K/Akt/eNOS pathway a mouse model of embryo implantation dysfunction.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Psychometric evaluation of the Depression Anxiety Stress Scale 8 among women with chronic non-cancer pelvic pain.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen (17β-oestradiol, E2) plays an essential role in endometrial receptivity and has been shown to stimulate angiogenesis via E2-ERα (estrogen receptor)-mediated upregulation of VEGF transcription. In this study, we have tried to decipher the mechanism of E2-promoting angiogenesis. We pre-incubated human endometrial microvascular endothelial cells (HEMECs) with E2 and performed western blotting, qRT-PCR, and cellular immunofluorescence experiments. We observed that E2 treatment of HEMECs increased ERα expression and reduced the expression of GRP78, which led to reduction of Caspase 3 expression by the CHOP pathway. In addition, E2 not only activated ERK signaling pathway but also inhibited p65 phosphorylation along with its translocation from nucleus to the cytoplasm, and subsequently inhibiting GRP78 expression, which led to inhibition of cell apoptosis. Together, these findings highlight the novel mechanism underlying E2-mediated improvement in endometrial angiogenesis through the ERK-p65 signaling pathway.
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Registered trials
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