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Correction: PPP2R2A inhibition contributes to preeclampsia by regulating the proliferation, apoptosis, and angiogenesis modulation potential of mesenchymal stem cells.

作者信息

Liu Yan, Gu Fangle, Gao Jun, Gu Yingyan, Li Zhiyue, Lu Dan, Zhang Yanxin

机构信息

Department of Obstetrics and Gynecology, Clinical Medical College, Yangzhou University, No. 98 Nantong West Road, Yangzhou, 225001, China.

出版信息

Cell Div. 2025 Jun 16;20(1):14. doi: 10.1186/s13008-025-00154-0.

DOI:10.1186/s13008-025-00154-0
PMID:40524258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12172283/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/93c191ad0ebb/13008_2025_154_Figd_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/ad8a75e4ae40/13008_2025_154_Figa_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/0bb034c023d2/13008_2025_154_Figb_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/66f40f03ad2b/13008_2025_154_Figc_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/93c191ad0ebb/13008_2025_154_Figd_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/ad8a75e4ae40/13008_2025_154_Figa_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/0bb034c023d2/13008_2025_154_Figb_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/66f40f03ad2b/13008_2025_154_Figc_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0625/12172283/93c191ad0ebb/13008_2025_154_Figd_HTML.jpg

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Correction: PPP2R2A inhibition contributes to preeclampsia by regulating the proliferation, apoptosis, and angiogenesis modulation potential of mesenchymal stem cells.更正：PPP2R2A抑制通过调节间充质干细胞的增殖、凋亡和血管生成调节潜能而导致子痫前期。
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本文引用的文献

1
ZEB2 reduction contributes to pre-eclampsia via Wnt/β-Catenin pathway.ZEB2表达降低通过Wnt/β-连环蛋白信号通路促使子痫前期的发生。
Cell Div. 2024 Nov 29;19(1):34. doi: 10.1186/s13008-024-00137-7.
2
PPP2R2A inhibition contributes to preeclampsia by regulating the proliferation, apoptosis, and angiogenesis modulation potential of mesenchymal stem cells.PPP2R2A抑制通过调节间充质干细胞的增殖、凋亡和血管生成调节潜能，导致子痫前期。
Cell Div. 2024 May 11;19(1):18. doi: 10.1186/s13008-024-00118-w.