Evidence map›Paper›PMID 36550096›Full record

ArticleCell death discovery2022

Elevated histone demethylase KDM5C increases recurrent miscarriage risk by preventing trophoblast proliferation and invasion.

Min Xiao, Yan Zheng, Meng-Xi Wang, Yi-Hua Sun, Juan Chen, Kang-Yong Zhu, Fan Zhang, Yun-Hui Tang, Fan Yang, Ting Zhou and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Min Xiao *Shanghai Ji Ai Genetics and IVF Institute, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.ORCID http://orcid.org/0000-0002-5720-5109
Yan Zheng *Department of Pancreatic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Meng-Xi Wang *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.ORCID http://orcid.org/0000-0002-4551-4326
Yi-Hua SunDepartment of Pathology, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
Juan ChenShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Kang-Yong ZhuShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Fan ZhangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Yun-Hui TangDepartment of Family Planning, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
Fan YangDepartment of Pathology, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
Ting ZhouDepartment of Orthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Yue-Ping ZhangShanghai Ji Ai Genetics and IVF Institute, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
Cai-Xia LeiShanghai Ji Ai Genetics and IVF Institute, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
Xiao-Xi SunShanghai Ji Ai Genetics and IVF Institute, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China. steven3019@hotmail.com.ORCID http://orcid.org/0000-0002-3366-5821
Shan-He YuShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China. yushanhe@shsmu.edu.cn.ORCID http://orcid.org/0000-0002-0268-7374
Fu-Ju TianThe International Peace Maternity & Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. fjtian@sibs.ac.cn.ORCID http://orcid.org/0000-0002-3638-8620
Shanghai Jiao Tong University · CNObstetrics and Gynecology Hospital of Fudan University · CNShangHai JiAi Genetics & IVF Institute · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071647
6 · The paper itself

Abstract

KDM5C is a histone H3K4-specific demethylase, which has been shown to play a key role in biological disease and development. However, the role of KDM5C in trophoblasts at early pregnancy is currently unknown. Here, we showed that KDM5C was upregulated in placental trophoblasts from recurrent miscarriage (RM) patients compared with healthy controls (HCs). Trophoblast proliferation and invasion was inhibited by KDM5C overexpression and was promoted by KDM5C knockdown. Transcriptome sequencing revealed that elevated KDM5C exerted anti-proliferation and anti-invasion effects by repressing the expression of essential regulatory genes. The combination analysis of RNA-seq, ChIP-seq and CUT&Tag assay showed that KDM5C overexpression leads to the reduction of H3K4me3 on the promoters and the corresponding downregulation of expression of several regulatory genes in trophoblasts. Among these genes, TGFβ2 and RAGE are essential for the proliferation and invasion of trophoblasts. Importantly, overexpression of KDM5C by a systemically delivered KDM5C adenovirus vector (Ad-KDM5C) promoted embryo resorption rate in mouse. Our results support that KDM5C is an important regulator of the trophoblast function during early pregnancy, and suggesting that KDM5C activity could be responsible for epigenetic alterations seen RM disease.

Identifiers

PMID36550096
PMCPMC9780362
OpenAlexW4312140959

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.