Evidence map›Paper›PMID 27079876›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

Vascular Actions of Angiotensin 1-7 in the Human Microcirculation: Novel Role for Telomerase.

Matthew J Durand, Natalya S Zinkevich, Michael Riedel, David D Gutterman, Victoria L Nasci, Valerie K Salato, John B Hijjawi, Charles F Reuben, Paula E North, Andreas M Beyer

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed, 62 citations in OpenAlex.

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  14. Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress.American journal of physiology. Heart and circulatory physiology · 2022
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  20. Endogenous Vasoactive Peptides and Vascular Aging-Related Diseases.Oxidative medicine and cellular longevity · 2022
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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

10 authors at 1 institution in 2 countries.

Matthew J DurandFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Natalya S ZinkevichFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Michael RiedelFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
David D GuttermanFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Victoria L NasciFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Valerie K SalatoFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
John B HijjawiFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Charles F ReubenFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Paula E NorthFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.).
Andreas M BeyerFrom the Department of Physical Medicine and Rehabilitation (M.J.D.), Department of Medicine, Cardiovascular Center (M.J.D., N.S.Z., M.R., D.D.G., V.L.N., A.M.B.), Department of Pathology, Division of Pediatric Pathology (V.K.S., P.E.N.), Department of Plastic Surgery (J.B.H.), Department of Cardiothoracic Surgery (C.F.R.), and Department of Physiology (A.M.B.), Medical College of Wisconsin, Milwaukee; and Department of Health and Medicine, Carroll University, Waukesha, WI (N.S.Z.). abeyer@mcw.edu.
Carroll University · US

Funding

HYPERTENSION TRAINING GRANTT32HL007792 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI HARDER, DAVID RAE · 1994 to 2013
$3.7M
Pivotal Role of Mitochondrial Telomerase in Regulation of Vascular Tone and Redox HomeostasisR01HL133029 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI BEYER, ANDREAS M · 2017 to 2021
$2.2M
Flow-Mediated Dilation of Human Coronary ArteriolesR01HL080704 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2006 to 2010
$1.8M
Mechanism of Flow-Induced Dilation in the Human MicrocirculationR01HL113612 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2013 to 2016
$1.7M
Role of Hydrogen Peroxide in the Mechanism of Flow-Induced Dilation of the Human R01HL094971 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2009 to 2012
$1.5M
Differentiation of mitochondrial vs. nuclear function of telomeraseR21OD018306 · OD · MEDICAL COLLEGE OF WISCONSIN · PI BEYER, ANDREAS M · 2014 to 2015
$411k
NHLBI NIH HHS R01 HL080704NHLBI NIH HHS R01 HL094971NHLBI NIH HHS R01 HL113612NHLBI NIH HHS R01 HL133029NHLBI NIH HHS T32 HL007792NIH HHS R21 OD018306
6 · The paper itself

Abstract

objectiveThis study examined vascular actions of angiotensin 1-7 (ANG 1-7) in human atrial and adipose arterioles. APPROACH AND

resultsThe endothelium-derived hyperpolarizing factor of flow-mediated dilation (FMD) switches from antiproliferative nitric oxide (NO) to proatherosclerotic hydrogen peroxide in arterioles from humans with coronary artery disease (CAD). Given the known vasoprotective properties of ANG 1-7, we tested the hypothesis that overnight ANG 1-7 treatment restores the NO component of FMD in arterioles from patients with CAD. Endothelial telomerase activity is essential for preserving the NO component of vasodilation in the human microcirculation; thus, we also tested whether telomerase activity was necessary for ANG 1-7-mediated vasoprotection by treating separate arterioles with ANG 1-7±the telomerase inhibitor 2-[[(2E)-3-(2-naphthalenyl)-1-oxo-2-butenyl1-yl]amino]benzoic acid. ANG 1-7 dilated arterioles from patients without CAD, whereas dilation was significantly reduced in arterioles from patients with CAD. In atrial arterioles from patients with CAD incubated with ANG 1-7 overnight, the NO synthase inhibitor NG-nitro-l-arginine methyl ester abolished FMD, whereas the hydrogen peroxide scavenger polyethylene glycol catalase had no effect. Conversely, in vessels incubated with ANG 1-7+2-[[(2E)-3-(2-naphthalenyl)-1-oxo-2-butenyl1-yl]amino]benzoic acid, NG-nitro-l-arginine methyl ester had no effect on FMD, but polyethylene glycol catalase abolished dilation. In cultured human coronary artery endothelial cells, ANG 1-7 significantly increased telomerase activity. These results indicate that ANG 1-7 dilates human microvessels, and dilation is abrogated in the presence of CAD. Furthermore, ANG 1-7 treatment is sufficient to restore the NO component of FMD in arterioles from patients with CAD in a telomerase-dependent manner.

conclusionsANG 1-7 exerts vasoprotection in the human microvasculature via modulation of telomerase activity.

Indexed as

Adipose TissueAgedAngiotensin IArteriolesCase-Control StudiesCells, CulturedCoronary Artery DiseaseCoronary VesselsDose-Response Relationship, DrugEndothelial CellsEnzyme InhibitorsFemaleHeart AtriaHumansIn Vitro TechniquesMaleAngiotensin Iangiotensin I (1-7)Enzyme InhibitorsNitric OxidePeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledTelomeraseTERT protein, humanVasodilator Agentscoronary artery diseasemicrocirculationnitric oxidetelomerasevasodilation

Identifiers

PMID27079876
PMCPMC4882242
OpenAlexW2577908441

What OpenQuestion holds

Textmetadata
LicenceTDM
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.