ArticleBiology open2020
Advanced oxidation protein products change biological behaviors of rat endometrial epithelial cells by activating ERK/P38 signaling pathways.
Article in Biology open, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Association of Free Radical Product and Polycystic Ovary Syndrome: A Systematic Review and Meta-analysis.Reproductive sciences (Thousand Oaks, Calif.) · 2024Pooled it
- May serum advanced oxidation protein products levels be diagnostic markers in endometrioma?BMC women's health · 2025Article
- Artificial Intelligence in Assessing Reproductive Aging: Role of Mitochondria, Oxidative Stress, and Telomere Biology.Diagnostics (Basel, Switzerland) · 2025Review
- Article
- Advanced oxidation protein products attenuate the autophagy-lysosome pathway in ovarian granulosa cells by modulating the ROS-dependent mTOR-TFEB pathway.Cell death & disease · 2024Article
- Accumulation of advanced oxidation protein products contributes to age-related impairment of gap junction intercellular communication in osteocytes of male mice.Bone & joint research · 2022Article
- Is There a Balance in Oxidative-Antioxidant Status in Blood Serum of Patients with Advanced Endometriosis?Antioxidants (Basel, Switzerland) · 2021Article
- Advanced Oxidation Protein Products Induce G1/G0-Phase Arrest in Ovarian Granulosa Cells via the ROS-JNK/p38 MAPK-p21 Pathway in Premature Ovarian Insufficiency.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced oxidation protein products (AOPPs) are a family of oxidized protein compounds and could induce oxidative stress and inflammatory lesion in various cells. The accumulation of AOPPs was associated with female reproductive diseases such as polycystic ovary syndrome (PCOS), leiomyoma and endometriosis. However, the relationship between AOPPs and endometrial cells is unclear. To explore the effects of accumulated AOPPs on endometrial cells, we treated normal rat endometrial epithelial cells (rEECs) and endometriosis model rats with AOPPs. Primary rEECs were collected from 8-week-old female Wistar rats. Increasing the amount of AOPPs in the media of rEECs enhanced rEEC proliferation and migration, and inhibited apoptosis. Moreover, AOPPs triggered the production of reactive oxygen species and nitrite along with activated ERK and P38 signal and this, in turn, led to an upregulation of proliferation and migration. With the treatment of antioxidants or the inhibitors of ERK and P38, the above effects of AOPPs on rEECs were attenuated. Additionally, in an endometriosis rat model, a similar phenomenon was observed in that the growth of endometriotic implants were promoted by AOPPs and EECs were significantly increased. This study indicated that the accumulation of AOPPs could promote rEEC proliferation and migration through ERK and P38 signal both
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