Evidence map›Paper›PMID 26536834›Full record

ArticleScientific reports2015

N-acetylcysteine inhibits in vivo oxidation of native low-density lipoprotein.

Yuqi Cui, Chandrakala A Narasimhulu, Lingjuan Liu, Qingbin Zhang, Patrick Z Liu, Xin Li, Yuan Xiao, Jia Zhang, Hong Hao, Xiaoyun Xie and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.5field-weighted citation impact, top 40% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  10. Antioxidants (Basel, Switzerland) · 2022
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  14. High-fat diet selectively decreases bone marrow linJournal of tissue engineering and regenerative medicine · 2020
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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

14 authors at 4 institutions in 2 countries.

Yuqi CuiDepartment of Cardiology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Chandrakala A NarasimhuluBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, USA.
Lingjuan LiuDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Qingbin ZhangDepartment of Cardiology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Patrick Z LiuDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Xin LiDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Yuan XiaoDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Jia ZhangDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Hong HaoDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Xiaoyun XieDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Guanglong HeDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Lianqun CuiDepartment of Cardiology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Sampath ParthasarathyBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, USA.
Zhenguo LiuDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
The Ohio State University Wexner Medical Center · USShandong University · CNFlorida College · USUniversity of Central Florida · US

Funding

Oxidized Low-density Lipoprotein Impairs Bone Marrow Stem Cell SurvivalR01HL124122 · NHLBI · OHIO STATE UNIVERSITY · PI LIU, ZHENGUO, ZHU, HUA · 2015 to 2018
$2.1M
Effects of Oxidized Low-density Lipoprotein on Bone Marrow Stem CellR01HL094650 · NHLBI · OHIO STATE UNIVERSITY · PI LIU, ZHENGUO · 2010 to 2014
$1.9M
NHLBI NIH HHS R01 HL094650NHLBI NIH HHS R01 HL124122NHLBI NIH HHS R01HL124122
6 · The paper itself

Abstract

Low-density lipoprotein (LDL) is non-atherogenic, while oxidized LDL (ox-LDL) is critical to atherosclerosis. N-acetylcysteine (NAC) has anti-atherosclerotic effect with largely unknown mechanisms. The present study aimed to determine if NAC could attenuate in vivo LDL oxidation and inhibit atherosclerosis. A single dose of human native LDL was injected intravenously into male C57BL/6 mice with and without NAC treatment. Serum human ox-LDL was detected 30 min after injection, reached the peak in 3 hours, and became undetectable in 12 hours. NAC treatment significantly reduced serum ox-LDL level without detectable serum ox-LDL 6 hours after LDL injection. No difference in ox-LDL clearance was observed in NAC-treated animals. NAC treatment also significantly decreased serum ox-LDL level in patients with coronary artery diseases and hyperlipidemia without effect on LDL level. Intracellular and extracellular reactive oxidative species (ROS) production was significantly increased in the animals treated with native LDL, or ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR(-/-)) mice that was effectively prevented with NAC treatment. NAC also significantly reduced atherosclerotic plaque formation in hyperlipidemic LDLR(-/-) mice. NAC attenuated in vivo oxidation of native LDL and ROS formation from ox-LDL associated with decreased atherosclerotic plaque formation in hyperlipidemia.

Indexed as

AcetylcysteineAnimalsAntioxidantsAtherosclerosisHumansHyperlipidemiasLipoproteins, LDLMaleMiceMice, Inbred C57BLOxidation-ReductionReactive Oxygen SpeciesReceptors, LDLAcetylcysteineAntioxidantsLipoproteins, LDLoxidized low density lipoproteinReactive Oxygen SpeciesReceptors, LDL

Identifiers

PMID26536834
PMCPMC4633729
OpenAlexW2193515894

What OpenQuestion holds

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LicenceCC BY
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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.