Evidence map›Paper›PMID 25721616›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2015

ACE2 and Ang-(1-7) protect endothelial cell function and prevent early atherosclerosis by inhibiting inflammatory response.

Yue-Hui Zhang, Yong-huan Zhang, Xue-Fei Dong, Qing-Qing Hao, Xiao-Ming Zhou, Qing-Tao Yu, Shu-Ying Li, Xu Chen, Abdulai Fallah Tengbeh, Bo Dong and 1 more

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
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  9. The RAAS Goodfellas in Cardiovascular System.Journal of clinical medicine · 2023
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11 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 1 country.

Yue-Hui ZhangDepartment of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Yong-huan Zhang
Xue-Fei Dong
Qing-Qing Hao
Xiao-Ming Zhou
Qing-Tao Yu
Shu-Ying Li
Xu Chen
Abdulai Fallah Tengbeh
Bo Dong
Yun Zhang
Shandong Provincial Hospital · CNShandong University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiotensin-converting enzyme 2 (ACE2) is a counter-regulator against ACE by converting angiotensin II (Ang-II) to Ang-(1-7), but the effect of ACE2 and Ang-(1-7) on endothelial cell function and atherosclerotic evolution is unknown. We hypothesized that ACE2 overexpression and Ang-(1-7) may protect endothelial cell function by counterregulation of angiotensin II signaling and inhibition of inflammatory response.

methodsWe used a recombinant adenovirus vector to locally overexpress ACE2 gene (Ad-ACE2) in human endothelial cells in vitro and in apoE-deficient mice in vivo. The Ang II-induced MCP-1, VCAM-1 and E-selectin expression, endothelial cell migration and adhesion of human monocytic cells (U-937) to HUVECs by ACE2 gene transfer were evaluated in vitro. Accelerated atherosclerosis was studied in vivo, and atherosclerosis was induced in apoE-deficient mice which were divided randomly into four groups that received respectively a ACE2 gene transfer, Ad-ACE2, Ad-EGFP, Ad-ACE2 + A779, an Ang-(1-7) receptor antagonist, control group. After a gene transfer for 4 weeks, atherosclerotic pathology was evaluated.

resultsACE2 gene transfer not only promoted HUVECs migration, inhibited adhesion of monocyte to HUVECs and decreased Ang II-induced MCP-1, VCAM-1 and E-selectin protein production in vitro, but also decreased the level of MCP-1, VCAM-1 and interleukin 6 and inhibit atherosclerotic plaque evolution in vivo. Further, administration of A779 increased the level of MCP-1, VCAM-1 and interleukin 6 in vivo and led to further advancements in atherosclerotic extent.

conclusionsACE2 and Ang-(1-7) significantly inhibit early atherosclerotic lesion formation via protection of endothelial function and inhibition of inflammatory response.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAngiotensin IIAnimalsApolipoproteins EAtherosclerosisCell AdhesionCell MovementChemokine CCL2Disease Models, AnimalEndothelium, VascularE-SelectinGene Transfer TechniquesHumansInflammationIn Vitro TechniquesACE2 protein, humanAce2 protein, mouseAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin IIApolipoproteins ECCL2 protein, humanCcl2 protein, mouseChemokine CCL2E-SelectinPeptide FragmentsPeptidyl-Dipeptidase AVascular Cell Adhesion Molecule-1

Identifiers

PMID25721616
OpenAlexW2155045770

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.