Evidence map›Paper›PMID 28684630›Full record

ArticleCirculation research2017

Sirt3 Impairment and SOD2 Hyperacetylation in Vascular Oxidative Stress and Hypertension.

Anna E Dikalova, Hana A Itani, Rafal R Nazarewicz, William G McMaster, Charles R Flynn, Roman Uzhachenko, Joshua P Fessel, Jorge L Gamboa, David G Harrison, Sergey I Dikalov

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 1 pooled it
10.6field-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.

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3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 1 synthesis or guideline pooled it, 297 citations in OpenAlex.

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  20. A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026
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120 more citing papers are in PubMed but not listed here.

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 1 country.

Anna E DikalovaFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Hana A ItaniFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Rafal R NazarewiczFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
William G McMasterFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Charles R FlynnFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Roman UzhachenkoFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Joshua P FesselFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Jorge L GamboaFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
David G HarrisonFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN.
Sergey I DikalovFrom the Division of Clinical Pharmacology (A.E.D., H.A.I., R.R.N., W.G.M., R.U., J.P.F., J.L.G., D.G.H., S.I.D.) and Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN. sergey.dikalov@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2016 to 2020
$12.4M
CLINICAL PHARMACOLOGY TRAINING PROGRAMT32GM007569 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Bjorn C Knollmann · 1985 to 2026
$12.4M
REGULATION OF VASCULAR FUNCTION BY THE ENDOTHELIUMR01HL039006 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 1987 to 2017
$5.5M
Sirtuin 3 Impairment and SOD2 Acetylation in Oxidative Stress and HypertensionR01HL124116 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DIKALOV, SERGEY · 2015 to 2018
$1.6M
The Role of The T Cell In The Genesis of Hypertension R01HL125865 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2015 to 2017
$1.2M
Mitochondrial Dysfunction in Chronic Kidney DiseaseK23DK100533 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GAMBOA, JORGE LUIS · 2013 to 2017
$763k
Metabolic Reprogramming in Pulmonary Arterial HypertensionK08HL121174 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI FESSEL, JOSHUA PATRICK · 2014 to 2018
$723k
LSM880-Airyscan Confocal Microscope for Large Shared ResourceS10OD021630 · OD · VANDERBILT UNIVERSITY · PI WELLS, K. SAM · 2016 to 2016
$560k
The Role of CD8 T Cells in HypertensionF32HL124972 · NHLBI · VANDERBILT UNIVERSITY · PI ITANI, HANA AHMAD · 2014 to 2015
$84k
NCRR NIH HHS UL1 RR024975NHLBI NIH HHS F32 HL124972NHLBI NIH HHS K08 HL121174NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL039006NHLBI NIH HHS R01 HL124116NHLBI NIH HHS R01 HL125865NIDDK NIH HHS K23 DK100533NIGMS NIH HHS T32 GM007569NIH HHS S10 OD021630
6 · The paper itself

Abstract

rationaleClinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels. Sirt3 impairment reduces the activity of a key mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2) because of hyperacetylation.

objectiveIn this study, we examined whether the loss of Sirt3 activity increases vascular oxidative stress because of SOD2 hyperacetylation and promotes endothelial dysfunction and hypertension. METHODS AND

resultsHypertension was markedly increased in Sirt3-knockout (Sirt3

conclusionsOur data suggest that diminished Sirt3 expression and redox inactivation of Sirt3 lead to SOD2 inactivation and contributes to the pathogenesis of hypertension.

Indexed as

AcetylationAnimalsCells, CulturedHumansHypertensionMiceMice, Inbred C57BLMice, KnockoutOxidative StressSirtuin 3Superoxide DismutaseSuperoxide Dismutase 2Sirt3 protein, mouseSirtuin 3Superoxide DismutaseSuperoxide Dismutase 2angiotensin IIanimalsblood pressurehypertensionmicemitochondriasuperoxide

Identifiers

PMID28684630
PMCPMC5562527
OpenAlexW2733051448

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Read underepoch 390

Registered trials

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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.