Evidence map›Paper›PMID 24799613›Full record

ArticleHypertension (Dallas, Tex. : 1979)2014

Angiotensin 1-7 reduces mortality and rupture of intracranial aneurysms in mice.

Ricardo A Peña Silva, David K Kung, Ian J Mitchell, Natalia Alenina, Michael Bader, Robson A S Santos, Frank M Faraci, Donald D Heistad, David M Hasan

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
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  5. RAAS in diabetic retinopathy: mechanisms and therapies.Archives of endocrinology and metabolism · 2024
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  17. An exploratory investigation of brain collateral circulation plasticity after cerebral ischemia in two experimental C57BL/6 mouse models.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Ricardo A Peña SilvaFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.). rpena@uniandes.edu.co david-hasan@uiowa.edu.
David K KungFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
Ian J MitchellFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
Natalia AleninaFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
Michael BaderFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
Robson A S SantosFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
Frank M FaraciFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
Donald D HeistadFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.).
David M HasanFrom the Departments of Internal Medicine (R.A.P.S., I.J.M., F.M.F., D.D.H.), Pharmacology (F.M.F., D.D.H.), and Neurosurgery (D.K.K., D.M.H.), University of Iowa; Facultad de Medicina, Universidad de los Andes, Bogotá, Colombia (R.A.P.S.); Max-Delbrück Center for Molecular Medicine, Berlin, Germany (N.A., M.B.); and Department of Physiology and Biophysics, Federal University of Minas Gerais, Minas Gerais, Brazil (R.A.S.S.). rpena@uniandes.edu.co david-hasan@uiowa.edu.
Universidade Federal de Minas Gerais · BRUniversidad de Los Andes · CO

Funding

Vascular Protection During HypertensionP01HL062984 · NHLBI · UNIVERSITY OF IOWA · PI HEISTAD, DONALD D · 2000 to 2015
$22.2M
MECHANISM AND IMPACT OF THALAMIC DYSFUNCTION AFTER CARDIAC ARRESTK08NS082362 · NINDS · WASHINGTON UNIVERSITY · PI SHOYKHET, MICHAEL · 2013 to 2017
$895k
Mechanisms of Effect of Aspirin on Cerebral Aneurysms in MiceK08NS082363 · NINDS · UNIVERSITY OF IOWA · PI HASAN, DAVID M. · 2013 to 2017
$846k
Aneurysm Sac Growth as the Etiology of Recurrence in Coiled Cerebral AneurysmsR03NS079227 · NINDS · UNIVERSITY OF IOWA · PI HASAN, DAVID M. · 2012 to 2013
$148k
Role of PPAR-gamma in Cerebral EndotheliumI01BX001399 · VA · IOWA CITY VA MEDICAL CENTER · PI FARACI, FRANK M · 2013 to 2018
–
BLRD VA I01 BX001399NHLBI NIH HHS HL-62984NHLBI NIH HHS P01 HL062984NINDS NIH HHS K08 NS082363NINDS NIH HHS NS082362NINDS NIH HHS R03 NS079227
6 · The paper itself

Abstract

Angiotensin II (Ang II) stimulates vascular inflammation, oxidative stress, and formation and rupture of intracranial aneurysms in mice. Because Ang 1-7 acts on Mas receptors and generally counteracts deleterious effects of Ang II, we tested the hypothesis that Ang 1-7 attenuates formation and rupture of intracranial aneurysms. Intracranial aneurysms were induced in wild-type and Mas receptor-deficient mice using a combination of Ang II-induced hypertension and intracranial injection of elastase in the basal cistern. Mice received elastase+Ang II alone or a combination of elastase+Ang II+Ang 1-7. Aneurysm formation, prevalence of subarachnoid hemorrhage, mortality, and expression of molecules involved in vascular injury were assessed. Systolic blood pressure was similar in mice receiving elastase+Ang II (mean±SE, 148±5 mm Hg) or elastase+Ang II+Ang 1-7 (144±5 mm Hg). Aneurysm formation was also similar in mice receiving elastase+Ang II (89%) or elastase+Ang II+Ang 1-7 (84%). However, mice that received elastase+Ang II+Ang 1-7 had reduced mortality (from 64% to 36%; P<0.05) and prevalence of subarachnoid hemorrhage (from 75% to 48%; P<0.05). In cerebral arteries, expression of the inflammatory markers, Nox2 and catalase increased similarly in elastase+Ang II or elastase+Ang II+Ang 1-7 groups. Ang 1-7 increased the expression of cyclooxygenase-2 and decreased the expression of matrix metalloproteinase-9 induced by elastase+Ang II (P<0.05). In Mas receptor-deficient mice, systolic blood pressure, mortality, and prevalence of subarachnoid hemorrhage were similar (P>0.05) in groups treated with elastase+Ang II or elastase+Ang II+Ang 1-7. The expression of Mas receptor was detected by immunohistochemistry in samples of human intracranial arteries and aneurysms. In conclusion, without attenuating Ang II-induced hypertension, Ang 1-7 decreased mortality and rupture of intracranial aneurysms in mice through a Mas receptor-dependent pathway.

Indexed as

Aneurysm, RupturedAngiotensin IAnimalsBlood PressureHumansIntracranial AneurysmMiceMice, KnockoutOxidative StressPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledAngiotensin Iangiotensin I (1-7)Peptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledangiotein (1–7)angiotensin (1–7) receptor Mas, humanhypertensionintracranial aneurysmsubarachnoid hemorrhage

Identifiers

PMID24799613
PMCPMC4096422
OpenAlexW2139839060

What OpenQuestion holds

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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.