Evidence map›Paper›PMID 31615657›Full record

ArticleBiochemical and biophysical research communications2019

Overexpression of myeloid angiotensin-converting enzyme (ACE) reduces atherosclerosis.

Derick Okwan-Duodu, Daiana Weiss, Zhenzi Peng, Luciana C Veiras, Duo-Yao Cao, Suguru Saito, Zakir Khan, Ellen A Bernstein, Jorge F Giani, W Robert Taylor and 1 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  13. Exploring the Impact of ACE Inhibition in Immunity and Disease.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022
    Review
  14. Article
  15. Novel roles of the renal angiotensin-converting enzyme.Molecular and cellular endocrinology · 2021
    Review
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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

11 authors at 3 institutions in 1 country.

Derick Okwan-DuoduDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Daiana WeissDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Zhenzi PengDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Luciana C VeirasDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Duo-Yao CaoDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Suguru SaitoDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Zakir KhanDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Ellen A BernsteinDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Jorge F GianiDepartment of Biomedical Sciences Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
W Robert TaylorDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA; Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA; Division of Cardiology, Atlanta VA Medical Center, Decatur, GA, USA.
Kenneth E BernsteinDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: kenneth.bernstein@cshs.org.
Cedars-Sinai Medical Center · USEmory University · USGeorgia Institute of Technology · US

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 2009 to 2019
$20.5M
The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2016 to 2020
$12.4M
Supplemental Grant: Increased neutrophil function in Alzheimer's diseaseR01AI134714 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2018 to 2021
$2.1M
The role of angiotensin-converting enzyme in renal inflammation, kidney injury and sodium retention during diabetic nephropathyR01HL142672 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2018 to 2021
$1.7M
Maladaptive Inflammation Impairs Collateral Vessel Formation in Sickle Cell DiseaseK99HL141638 · NHLBI · EMORY UNIVERSITY · PI OKWAN-DUODU, DERICK · 2019 to 2020
$210k
NHLBI NIH HHS K99 HL141638NHLBI NIH HHS P01 HL095070NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL142672NIAID NIH HHS R01 AI134714
6 · The paper itself

Abstract

backgroundMacrophages are ubiquitous in all stages of atherosclerosis, exerting tremendous impact on lesion progression and plaque stability. Because macrophages in atherosclerotic plaques express angiotensin-converting enzyme (ACE), current dogma posits that local myeloid-mediated effects worsen the disease. In contrast, we previously reported that myeloid ACE overexpression augments macrophage resistance to various immune challenges, including tumors, bacterial infection and Alzheimer's plaque deposition. Here, we sought to assess the impact of myeloid ACE on atherosclerosis.

methodsA mouse model in which ACE is overexpressed in myelomonocytic lineage cells, called ACE10, was generated and sequentially crossed with ApoE-deficient mice to create ACE

resultsWith an atherogenic diet alone or in combination with DOCA, the ACE10/ApoE mice showed significantly less atherosclerotic plaques compared to their WT/ApoE counterparts (p < 0.01). When recipient ApoE

conclusionOur data indicate that while myeloid ACE may not be required for atherosclerosis, enhanced ACE expression paradoxically reduced disease progression.

Indexed as

AnimalsAtherosclerosisBlood PressureBone Marrow TransplantationCell LineageCholesterolDiet, AtherogenicDisease Models, AnimalDisease ProgressionHumansMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout, ApoEMyeloid CellsCholesterolPeptidyl-Dipeptidase AAngiotensin-converting enzymeAtherosclerosisHypertensionInflammationMyeloid cells

Identifiers

PMID31615657
PMCPMC6916669
OpenAlexW2979731087

What OpenQuestion 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 OpenQuestion graph.