Evidence map›Paper›PMID 29379093›Full record

ArticleScientific reports2018

MCPIP1-induced autophagy mediates ischemia/reperfusion injury in endothelial cells via HMGB1 and CaSR.

Xiaolong Xie, Tiebing Zhu, Lulu Chen, Shuang Ding, Han Chu, Jing Wang, Honghong Yao, Jie Chao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026
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  11. High-Mobility Group Box 1 (HMGB1) and Autophagy in Acute Lung Injury (ALI): A Review.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Review
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 2 countries.

Xiaolong XieDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, China.
Tiebing ZhuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, China. jyfz15117@sina.com.
Lulu ChenDepartment of Physiology, Medical School of Southeast University, Nanjing, Jiangsu, 210009, China.
Shuang DingDepartment of Physiology, Medical School of Southeast University, Nanjing, Jiangsu, 210009, China.
Han ChuDepartment of Physiology, Medical School of Southeast University, Nanjing, Jiangsu, 210009, China.
Jing WangDepartment of Physiology, Medical School of Southeast University, Nanjing, Jiangsu, 210009, China.
Honghong YaoDepartment of Pharmacology, School of Medicine, Southeast University, Nanjing, Jiangsu, 210009, China.
Jie ChaoDepartment of Physiology, Medical School of Southeast University, Nanjing, Jiangsu, 210009, China. chaojie@seu.edu.cn.ORCID http://orcid.org/0000-0002-7800-3557
Southeast University · CNJiangsu Province Hospital · CNSoutheast University · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocyte chemotactic protein-1-induced protein 1 (MCPIP1) plays a important role in ischemia/reperfusion (I/R) injury. Autophagy is involved in activating endothelial cells in response to I/R. However, researchers have not clearly determined whether MCPIP1 mediates I/R injury in endothelial cells via autophagy, and its downstream mechanism remains unclear. Western blotting analyses and immunocytochemistry were applied to detect protein levels were detected in HUVECs. An in vitro scratch assay was used to detect cell migration. Cells were transfected with siRNAs to knockdown MCPIP1 and high mobility group box 1 (HMGB1) expression. The pharmacological activator of autophagy rapamycin and the specific calcium-sensing receptor (CaSR) inhibitor NPS-2143 were used to confirm the roles of autophagy and CaSR in I/R injury. I/R induced HMGB1 and CaSR expression, which subsequently upreguated the migration and apoptosis of HUVECs and coincided with the increase of autophagy. HMGB1 was involved in cell migration, whereas CaSR specifically participated in I/R-induced HUVEC apoptosis. Based on these findings, I/R-induced MCPIP1 expression regulates the migration and apoptosis of HUVECs via HMGB1 and CaSR, respectively, suggesting a new therapeutic targetof I/R injury.

Indexed as

AutophagyBlotting, WesternCell MovementCells, CulturedEndothelial CellsGene Expression RegulationGene Knockdown TechniquesHMGB1 ProteinHumansImmunohistochemistryReceptors, Calcium-SensingReperfusion InjuryRibonucleasesTranscription FactorsCASR protein, humanHMGB1 ProteinReceptors, Calcium-SensingRibonucleasesTranscription FactorsZC3H12A protein, human

Identifiers

PMID29379093
PMCPMC5788920
OpenAlexW2800733174

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.