Evidence map›Paper›PMID 31901211›Full record

ReviewClinical and experimental pharmacology & physiology2020

The potential actions of angiotensin-converting enzyme II (ACE2) activator diminazene aceturate (DIZE) in various diseases.

Tawar Qaradakhi, Laura Kate Gadanec, Kristen Renee McSweeney, Alexander Tacey, Vasso Apostolopoulos, Itamar Levinger, Kvetoslava Rimarova, Emmanuel E Egom, Luis Rodrigo, Peter Kruzliak and 2 more

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental pharmacology & physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
12.0field-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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

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  6. Analysis of modifying factors for ACE2 to work effectively.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 7 institutions in 5 countries.

Tawar QaradakhiInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Laura Kate GadanecInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Kristen Renee McSweeneyInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Alexander TaceyInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Vasso ApostolopoulosInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Itamar LevingerInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Kvetoslava RimarovaDepartment of Public Health and Hygiene, Faculty of Medicine, Pavol Jozef Safarik University, Kosice, Slovakia.
Emmanuel E EgomEgom Clinical & Translational Research Services Ltd, Dartmouth, NS, Canada.
Luis RodrigoFaculty of Medicine, University of Oviedo and Central University Hospital of Asturias (HUCA), Oviedo, Spain.
Peter KruzliakDepartment of Internal Medicine, Borthers of Mercy Hospital, Brno, Czech Republic.ORCID 0000-0002-7069-3784
Peter KubatkaDepartment of Medical Biology, Jessenius Faculty of Medicine, Comenius University in Bratislava, Martin, Slovakia.
Anthony ZulliInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Victoria University · AUWestern Health · AUComenius University Bratislava · SKJewish General Hospital · CAMasaryk University · CZUniversidad de Oviedo · ESUniversity of Pavol Jozef Šafárik · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The renin angiotensin system (RAS) regulates fluid balance, blood pressure and maintains vascular tone. The potent vasoconstrictor angiotensin II (Ang II) produced by angiotensin-converting enzyme (ACE) comprises the classical RAS. The non-classical RAS involves the conversion of Ang II via ACE2 into the vasodilator Ang (1-7) to counterbalance the effects of Ang II. Furthermore, ACE2 converts AngA into another vasodilator named alamandine. The over activation of the classical RAS (increased vasoconstriction) and depletion of the non-classical RAS (decreased vasodilation) results in vascular dysfunction. Vascular dysfunction is the leading cause of atherosclerosis and cardiovascular disease (CVD). Additionally, local RAS is expressed in various tissues and regulates cellular functions. RAS dysregulation is involved in other several diseases such as inflammation, renal dysfunction and even cancer growth. An approach in restoring vascular dysfunction and other pathological diseases is to either increase the activity of ACE2 or reduce the effect of the classical RAS by counterbalancing Ang II effects. The antitrypanosomal agent, diminazene aceturate (DIZE), is one approach in activating ACE2. DIZE has been shown to exert beneficial effects in CVD experimental models of hypertension, myocardial infarction, type 1 diabetes and atherosclerosis. Thus, this review focuses on DIZE and its effect in several tissues such as blood vessels, cardiac, renal, immune and cancer cells.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsCardiovascular DiseasesDiminazeneEnzyme ActivationEnzyme ActivatorsHumansNeoplasmsRenin-Angiotensin SystemACE2 protein, humanAngiotensin-Converting Enzyme 2Diminazenediminazene aceturateEnzyme Activatorsangiotensin-converting enzyme IIcardiovascular diseasediminazene aceturateendothelial dysfunctionrenin angiotensin system

Identifiers

PMID31901211
OpenAlexW2997366394

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.