Evidence map›Paper›PMID 31111864›Full record

ArticleAmerican journal of hypertension2019

PKC-Mediated Endothelin-1 Expression in Endothelial Cell Promotes Macrophage Activation in Atherogenesis.

Juan Zhang, Yan-Jiang Wang, Xin Wang, Lin Xu, Xin-Chun Yang, Wen-Shu Zhao

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in American journal of hypertension, 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
1.0field-weighted citation impact, top 25% 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, 27 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. Endothelin-1 in Health and Disease.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. A Visualization Analysis of Global Research Trends in Studies of Lower Extremity Arteriosclerosis Obliterans Prognosis (1942-2025).Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Juan ZhangCardiac Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Yan-Jiang WangCardiac Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Xin WangCardiac Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Lin XuCardiac Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Xin-Chun YangCardiac Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Wen-Shu ZhaoCardiac Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Capital Medical University · CNBeijing Chao-Yang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis is a chronic inflammatory disease triggered by endothelial dysfunction and exaggerated by macrophage infiltration. Although endothelin-1 (ET-1) plays an important role in vascular inflammation and reactive oxygen species production, the individual effect of ET-1 in atherogenesis remains unclear. METHODS AND

resultsET-1 expression was increased in mouse atherosclerotic plaques and human umbilical vein endothelial cells (HUVECs) administrated by oxidized low-density lipoprotein stimulation. Moreover, the immunofluorescence co-staining showed upregulated ET-1 expression in endothelial cells. Real-time polymerase chain reaction demonstrated that ET-1 overexpression promoted adhesion molecules and chemokines secretion in HUVECs. Following this intervention, the migration of macrophages and the pro-inflammatory cytokines were increased. More importantly, the endothelial dysfunction regulated by ET-1 and subsequently the effect on macrophage activation were mediated by ETA receptor and largely reversed by protein kinase C (PKC) inhibitor. Eight-week-old male ApoE-/- mice and eET-1/ApoE-/- mice were fed with high-fat diet for 12 weeks. eET-1/ApoE-/- significantly increased atherosclerotic lesions in the whole aorta and aortic sinus, which accompanied by the induction of inflammatory cytokines and macrophages infiltration.

conclusionsET-1 accelerates atherogenesis by promoting adhesion molecules and chemokines, as well as subsequent macrophage activation. Collected, these evidence suggest that ET-1 might be a potential target for the treatment of atherogenesis.

Indexed as

Macrophage ActivationParacrine CommunicationAnimalsAtherosclerosisCell Adhesion MoleculesCell MovementCytokinesDisease Models, AnimalEndothelial CellsEndothelin-1HumansHuman Umbilical Vein Endothelial CellsInflammation MediatorsMacrophagesMaleMiceCell Adhesion MoleculesCytokinesEDNRA protein, humanEndothelin-1Inflammation MediatorsProtein Kinase CReceptor, Endothelin Aatherosclerosisblood pressureendothelial-1HUVECshypertensionmacrophagesPKC

Identifiers

PMID31111864
OpenAlexW2946743807

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.