Evidence map›Paper›PMID 24429674›Full record

ArticleAmerican journal of hypertension2014

Autocrine and paracrine function of Angiotensin 1-7 in tissue repair during hypertension.

Weixin Meng, Wenyuan Zhao, Tieqiang Zhao, Chang Liu, Yuanjian Chen, Hongyu Liu, Yao Sun

Open access · bronzeAbstract read
In one paragraph

Article in American journal of hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-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

20 citing papers in PubMed, 35 citations in OpenAlex.

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  6. Disequilibrium between the classic renin-angiotensin system and its opposing arm in SARS-CoV-2-related lung injury.American journal of physiology. Lung cellular and molecular physiology · 2020
    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

7 authors at 2 institutions in 2 countries.

Weixin MengDivision of Cardiac Surgery, Department of Surgery, First Affiliate Hospital of Harbin Medical University, Harbin, China.
Wenyuan Zhao
Tieqiang Zhao
Chang Liu
Yuanjian Chen
Hongyu Liu
Yao Sun
First Affiliated Hospital of Harbin Medical University · CNUniversity of Tennessee Health Science Center · US

Funding

Regulatory Mechanisms of Oxidative Stress in Cardiac Angiogenesis PostinfarctionR01HL096503 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, YAO · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL096503NHLBI NIH HHS R01- HL096503
6 · The paper itself

Abstract

backgroundAngiotensin-converting enzyme 2 (ACE2) cleaves angiotensin (Ang) II to generate Ang1-7, which mediates cellular actions through Mas receptors (MasR). Hypertension is accompanied by high or low circulating AngII levels and cardiac/renal injury. The purpose of this study is to explore (i) whether circulating AngII affects ACE2/MasR expressions in the hypertensive heart and kidney; and (ii) whether Ang1-7 regulates cardiac repair/remodeling responses through MasR during hypertension.

methodsIn the first portion of the study, rats received either an AngII infusion (400ng/kg/min) for 4 weeks, leading to hypertension with high circulating AngII, or an aldosterone (ALDO, 0.75 μg/h) infusion for 4 weeks, leading to hypertension with low/normal circulating AngII. Cardiac and renal ACE2/MasR expressions were examined. We found that cardiac ACE2 was increased and MasR attenuated in both AngII and ALDO groups. However, renal ACE2 and MasR remained unchanged in both AngII- and ALDO-treated animals.

resultsIn the second portion, rats received AngII infusion with/without MasR antagonist (A779, 1mg/kg/day) for 4 weeks. The roles of MasR blockade in cardiac inflammation, fibrosis, apoptosis, and ventricular function were examined. Chronic AngII infusion caused scattered cardiac injuries, and A779 cotreatment exacerbated cardiac injury, resulting in aggravated inflammatory, fibrogenic, and apoptotic responses compared with the AngII group. Cardiac function, however, was unaltered in the AngII and A779 groups.

conclusionsACE2 and MasR expressions in the hypertensive heart and kidney are not regulated by circulating AngII levels. Ang1-7 is involved in multiple repair responses, suggesting that therapeutic strategies aimed at administering Ang1-7 hold potential for the management of cardiac remodeling.

Indexed as

Autocrine CommunicationParacrine CommunicationVentricular RemodelingAldosteroneAngiotensin-Converting Enzyme 2Angiotensin IAngiotensin IIAnimalsApoptosisDisease Models, AnimalFibrosisHypertensionKidneyMaleMyocardiumPeptide Fragments7-Ala-angiotensin (1-7)Ace2 protein, ratAldosteroneAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin IIPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledangiotensin 1–7blood pressurehearthypertensionkidneyMas receptor blockaderepair.

Identifiers

PMID24429674
PMCPMC4017929
OpenAlexW2106985110

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.