Evidence map›Paper›PMID 26318157›Full record

ArticleJournal of lipid research2015

Hepatic overexpression of methionine sulfoxide reductase A reduces atherosclerosis in apolipoprotein E-deficient mice.

Yan-Yong Xu, Fen Du, Bing Meng, Guang-Hui Xie, Jia Cao, Daping Fan, Hong Yu

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Yan-Yong XuDepartment of Biochemistry and Molecular Biology Wuhan University School of Basic Medical Sciences, Wuhan, China.
Fen DuDepartment of Biochemistry and Molecular Biology Wuhan University School of Basic Medical Sciences, Wuhan, China Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University School of Basic Medical Sciences, Wuhan, China Department of Cell Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC.
Bing MengDepartment of Biochemistry and Molecular Biology Wuhan University School of Basic Medical Sciences, Wuhan, China.
Guang-Hui XieDepartment of Biochemistry and Molecular Biology Wuhan University School of Basic Medical Sciences, Wuhan, China.
Jia CaoDepartment of Biochemistry and Molecular Biology Wuhan University School of Basic Medical Sciences, Wuhan, China.
Daping FanDepartment of Cell Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC.
Hong YuDepartment of Biochemistry and Molecular Biology Wuhan University School of Basic Medical Sciences, Wuhan, China Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Wuhan University · CNUniversity of South Carolina · US

Funding

Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI CHATTERJEE, SAURABH · 2007 to 2018
$14.2M
Sparstolonin B as an anti-atherogenic agentR01HL116626 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FAN, DAPING · 2013 to 2017
$1.7M
NCCIH NIH HHS P01 AT003961NHLBI NIH HHS HL116626NHLBI NIH HHS R01 HL116626
6 · The paper itself

Abstract

Methionine sulfoxide reductase A (MsrA), a specific enzyme that converts methionine-S-sulfoxide to methionine, plays an important role in the regulation of protein function and the maintenance of redox homeostasis. In this study, we examined the impact of hepatic MsrA overexpression on lipid metabolism and atherosclerosis in apoE-deficient (apoE(-/-)) mice. In vitro study showed that in HepG2 cells, lentivirus-mediated human MsrA (hMsrA) overexpression upregulated the expression levels of several key lipoprotein-metabolism-related genes such as liver X receptor α, scavenger receptor class B type I, and ABCA1. ApoE(-/-) mice were intravenously injected with lentivirus to achieve high-level hMsrA expression predominantly in the liver. We found that hepatic hMsrA expression significantly reduced plasma VLDL/LDL levels, improved plasma superoxide dismutase, and paraoxonase-1 activities, and decreased plasma serum amyloid A level in apoE(-/-) mice fed a Western diet, by significantly altering the expression of several genes in the liver involving cholesterol selective uptake, conversion and excretion into bile, TG biosynthesis, and inflammation. Moreover, overexpression of hMsrA resulted in reduced hepatic steatosis and aortic atherosclerosis. These results suggest that hepatic MsrA may be an effective therapeutic target for ameliorating dyslipidemia and reducing atherosclerosis-related cardiovascular diseases.

Indexed as

AnimalsApolipoproteins EAtherosclerosisCells, CulturedCholesterolHep G2 CellsHumansLipid MetabolismLiverMaleMethionine Sulfoxide ReductasesMiceMice, Inbred C57BLMice, KnockoutReceptors, LDLApolipoproteins ECholesterolMethionine Sulfoxide ReductasesReceptors, LDLantioxidantscholesterol effluxcholesterol eliminationinflammationlipoprotein metabolismlipoprotein receptorsparaoxonase-1

Identifiers

PMID26318157
PMCPMC4583078
OpenAlexW2176384544

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.