Evidence map›Paper›PMID 31399951›Full record

ArticleJournal of physiology and biochemistry2019

Dysregulated expression of ACTN4 contributes to endothelial cell injury via the activation of the p38-MAPK/p53 apoptosis pathway in preeclampsia.

Jianlin Zhao, Wei Peng, Yuxin Ran, Huisheng Ge, Chen Zhang, Hong Zou, Yubin Ding, Hongbo Qi

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 37 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

8 authors at 3 institutions in 1 country.

Jianlin ZhaoDepartment of Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Wei PengDepartment of Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yuxin RanDepartment of Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Huisheng GeDepartment of Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Chen ZhangDepartment of Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Hong ZouDepartment of Obstetrics, University-Town Hospital of Chongqing Medical University, Chongqing, 401331, China.
Yubin DingInternational Collaborative Laboratory of Reproduction and Development of Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Hongbo QiDepartment of Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. qihongbocy@gmail.com.
Children's Hospital of Chongqing Medical University · CNChongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

National Key Research and Development Program the research on birth defect prevention and control of reproductive health special emphasis 2016YFC1000407National Natural Science Foundation of China 81520108013, 81471472, 81771613, 81501286, 81601304, 81701479, 81701480, 81801482the Key Program of International Cooperation of NSFC 81520108013
6 · The paper itself

Abstract

Preeclampsia (PE) is a hypertensive disease associated with increased endothelial cell dysfunction caused by systemic oxidative stress. Alpha-actinin-4 (ACTN4) is a member of the α-actinin family of actin crosslinking proteins that are upregulated in several types of cancer. However, its role in PE remains unclear. In this study, we found that ACTN4 was localized in placenta vascular endothelial cells (ECs), and its expression was downregulated in primary human umbilical vein endothelial cells (HUVECs) from severe preeclamptic patients compared to that in HUVECs from normotensive pregnant women. ACTN4 expression was also decreased in normotensive HUVECs treated with H

Indexed as

ApoptosisOxidative StressActininAdultCaspasesFemaleHumansHuman Umbilical Vein Endothelial CellsHydrogen Peroxidep38 Mitogen-Activated Protein KinasesPre-EclampsiaPregnancyReactive Oxygen SpeciesTumor Suppressor Protein p53Young AdultActininACTN4 protein, humanCaspasesHydrogen Peroxidep38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTumor Suppressor Protein p53ApoptosisEndothelial cell dysfunctionOxidative stressP38-MAPK/p53 pathwayPreeclampsia

Identifiers

PMID31399951
OpenAlexW2967791276

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.