Evidence map›Paper›PMID 26422756›Full record

ArticleAntioxidants & redox signaling2016

SIRT3 Mediates the Antioxidant Effect of Hydrogen Sulfide in Endothelial Cells.

Liping Xie, Haihua Feng, Sha Li, Guoliang Meng, Shangmin Liu, Xin Tang, Yan Ma, Yi Han, Yujiao Xiao, Yue Gu and 9 more

Open access · greenAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 109 citations in OpenAlex.

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  9. The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023
    Review
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  11. Advances of HAntioxidants (Basel, Switzerland) · 2023
    Review
  12. Comparative Study of Different HAntioxidants (Basel, Switzerland) · 2023
    Article
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  17. The CBS-HBritish journal of cancer · 2022
    Article
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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

19 authors at 5 institutions in 3 countries.

Liping Xie1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Haihua Feng1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Sha Li1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Guoliang Meng1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Shangmin Liu1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Xin Tang1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Yan Ma1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Yi Han3 Department of Geriatrics, the First Affiliated Hospital of Nanjing Medical University , Nanjing, China .
Yujiao Xiao1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Yue Gu1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Yongfeng Shao4 Department of Cardiothoracic Surgery, the First Affiliated Hospital of Nanjing Medical University , Nanjing, China .
Chung-Min Park5 Department of Chemistry, Washington State University , Pullman, Washington.
Ming Xian5 Department of Chemistry, Washington State University , Pullman, Washington.
Yu Huang6 Institute of Vascular Biology, Chinese University of Hong Kong , Hong Kong, China .
Albert Ferro7 Cardiovascular Division, Department of Clinical Pharmacology, School of Medicine, King's College London , London, United Kingdom .
Rui Wang8 Department of Biology, Cardivascular and Molecular Research Unit, Lakehead University , Thunder Bay, Ontario, Canada .
Philip K Moore9 Department of Pharmacology, National University of Singapore , Singapore .
Hong Wang10 Department of Pharmacology, Center for Metabolic Disease Research, Temple University School of Medicine , Philadelphia, Pennsylvania.
Yong Ji1 Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University , Nanjing, China .
Nanjing Medical University · CNJiangsu Province Hospital · CNWashington State University · USNantong University · CNNational University of Singapore · SG

Funding

Atherogenic mechanisms with homocysteineR01HL077288 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2004 to 2014
$3.8M
NADHP Oxidase-mediated MC differentiation & Endothelial Dysfunction in HHcyR01HL110764 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2011 to 2015
$2.5M
Novel Sulfide Releasing Agents for Ischemic InjuryR01HL116571 · NHLBI · WASHINGTON STATE UNIVERSITY · PI LEFER, DAVID JOSEPH, XIAN, MING · 2014 to 2017
$1.8M
NHLBI NIH HHS R01 HL077288NHLBI NIH HHS R01 HL110764NHLBI NIH HHS R01HL116571
6 · The paper itself

Abstract

aimOxidative stress is a key contributor to endothelial dysfunction and associated cardiovascular pathogenesis. Hydrogen sulfide (H2S) is an antioxidant gasotransmitter that protects endothelial cells against oxidative stress. Sirtuin3 (SIRT3), which belongs to the silent information regulator 2 (SIR2) family, is an important deacetylase under oxidative stress. H2S is able to regulate the activity of several sirtuins. The present study aims to investigate the role of SIRT3 in the antioxidant effect of H2S in endothelial cells.

resultsCultured EA.hy926 endothelial cells were exposed to hydrogen peroxide (H2O2) as a model of oxidative stress-induced cell injury. GYY4137, a slow-releasing H2S donor, improved cell viability, reduced oxidative stress and apoptosis, and improved mitochondrial function following H2O2 treatment. H2S reversed the stimulation of MAPK phosphorylation, downregulation of SIRT3 mRNA and reduction of the superoxide dismutase 2 and isocitrate dehydrogenase 2 expression which were induced by H2O2. H2S also increased activator protein 1 (AP-1) binding activity with SIRT3 promoter and this effect was absent in the presence of the specific AP-1 inhibitor, SR11302 or curcumin. Paraquat administration to mice induced a defected endothelium-dependent aortic vasodilatation and increased oxidative stress in both mouse aorta and small mesenteric artery, which were alleviated by GYY4137 treatment. This vasoprotective effect of H2S was absent in SIRT3 knockout mice. INNOVATION: The present results highlight a novel role for SIRT3 in the protective effect of H2S against oxidant damage in the endothelium both in vitro and in vivo.

conclusionH2S enhances AP-1 binding activity with the SIRT3 promoter, thereby upregulating SIRT3 expression and ultimately reducing oxidant-provoked vascular endothelial dysfunction. Antioxid. Redox Signal. 24, 329-343.

Indexed as

AnimalsAntioxidantsCell LineCell SurvivalChromatin ImmunoprecipitationEndothelial CellsHydrogen PeroxideHydrogen SulfideMembrane Potential, MitochondrialMiceMice, Mutant StrainsOxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionSirtuin 3AntioxidantsHydrogen PeroxideHydrogen SulfideReactive Oxygen SpeciesSirtuin 3

Identifiers

PMID26422756
PMCPMC4761821
OpenAlexW2116268698

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.