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Copyright (c) 2024 Feng Zhang, Bing Zhang, Tingting Yin, Fangbo Qian, Bin Lu, Weipei Zhu
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.The molecular mechanism of ferroptosis-induced spontaneous abortion based on bioinformatics approach
Corresponding Author(s) : Weipei Zhu
Cellular and Molecular Biology,
Vol. 70 No. 8: Issue 8
Abstract
Spontaneous abortion (SA) is a prevalent placental dysfunction, and ferroptosis may play a crucial role in placental dysfunction and the development of SA. In this study, we employed data mining and analysis techniques to investigate the biological mechanism of SA induced by ferroptosis, resulting in the identification of a total of 79 ferroptosis-related genes in SA were identified. Among them, 3 co-expression modules of ferroptosis risk genes, ten significant functions and six biologically significant pathways were obtained 61 pairs of differentially expressed miRNA-ferroptosis factor relationships were identified, and WIPI1 and GSN were expressed at significantly higher levels in SA. This is extremely helpful for future research on SA.
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