Evidence map›Paper›PMID 38569496›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Thrombospondin-1 Regulates Trophoblast Necroptosis via NEDD4-Mediated Ubiquitination of TAK1 in Preeclampsia.

Haoyue Hu, Jing Ma, You Peng, Rixuan Feng, Chenling Luo, Minyi Zhang, Zixin Tao, Lu Chen, Tao Zhang, Wenqian Chen and 6 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 20 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

16 authors at 4 institutions in 3 countries.

Haoyue HuDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.ORCID 0000-0003-2706-0321
Jing MaDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
You PengDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Rixuan FengSchool of Nursing, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Chenling LuoSchool of Nursing, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Minyi ZhangDepartment of Epidemiology, School of Public Health, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Zixin TaoDepartment of Obstetrics and Gynecology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, 510180, China.
Lu ChenDepartment of Obstetrics and Gynaecology;, Li Ka Shing Institute of Health Sciences;, School of Biomedical Sciences;, Chinese University of Hong Kong-Sichuan University Joint Laboratory in Reproductive Medicine; The Chinese University of Hong Kong, Hong Kong SAR, NT, China.
Tao ZhangDepartment of Obstetrics and Gynaecology;, Li Ka Shing Institute of Health Sciences;, School of Biomedical Sciences;, Chinese University of Hong Kong-Sichuan University Joint Laboratory in Reproductive Medicine; The Chinese University of Hong Kong, Hong Kong SAR, NT, China.
Wenqian ChenDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Qian YinDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Jinguo ZhaiSchool of Nursing, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Jun ChenDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Ailan YinDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Chi Chiu WangDepartment of Obstetrics and Gynaecology;, Li Ka Shing Institute of Health Sciences;, School of Biomedical Sciences;, Chinese University of Hong Kong-Sichuan University Joint Laboratory in Reproductive Medicine; The Chinese University of Hong Kong, Hong Kong SAR, NT, China.
Mei ZhongDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.ORCID 0000-0002-5848-8219
Nanfang Hospital · CNSouthern Medical University · CNChinese University of Hong Kong · HKGuangzhou First People's Hospital · CN

Funding

China Postdoctoral Science Foundation 2022M721501Guangzhou Health Science and Technology Project 2023A031001Ministry of Science and Technology of China (MOST) 2021YFC2701603Nanfang Hospital 2022B012National Natural Science Foundation of China 82301913
6 · The paper itself

Abstract

Preeclampsia (PE) is considered as a disease of placental origin. However, the specific mechanism of placental abnormalities remains elusive. This study identified thrombospondin-1 (THBS1) is downregulated in preeclamptic placentae and negatively correlated with blood pressure. Functional studies show that THBS1 knockdown inhibits proliferation, migration, and invasion and increases the cycle arrest and apoptosis rate of HTR8/SVneo cells. Importantly, THBS1 silencing induces necroptosis in HTR8/SVneo cells, accompanied by the release of damage-associated molecular patterns (DAMPs). Necroptosis inhibitors necrostatin-1 and GSK'872 restore the trophoblast survival while pan-caspase inhibitor Z-VAD-FMK has no effect. Mechanistically, the results show that THBS1 interacts with transforming growth factor B-activated kinase 1 (TAK1), which is a central modulator of necroptosis quiescence and affects its stability. Moreover, THBS1 silencing up-regulates the expression of neuronal precursor cell-expressed developmentally down-regulated 4 (NEDD4), which acts as an E3 ligase of TAK1 and catalyzes K48-linked ubiquitination of TAK1 in HTR8/SVneo cells. Besides, THBS1 attenuates PE phenotypes and improves the placental necroptosis in vivo. Taken together, the down-regulation of THBS1 destabilizes TAK1 by activating NEDD4-mediated, K48-linked TAK1 ubiquitination and promotes necroptosis and DAMPs release in trophoblast cells, thus participating in the pathogenesis of PE.

Indexed as

MAP Kinase Kinase KinasesNecroptosisNedd4 Ubiquitin Protein LigasesPre-EclampsiaThrombospondin 1TrophoblastsUbiquitinationAdultFemaleHumansMAP Kinase Kinase Kinase 7PlacentaPregnancyMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNedd4 protein, humanNedd4 Ubiquitin Protein LigasesThrombospondin 1thrombospondin-1, humannecroptosispreeclampsiathrombospondin‐1trophoblastubiquitination

Identifiers

PMID38569496
PMCPMC11151050
OpenAlexW4393852051

What Socratic holds

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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 Socratic graph.