Evidence map›Paper›PMID 22548251›Full record

ArticleAntioxidants & redox signaling2012

Overexpression of peroxiredoxin 4 attenuates atherosclerosis in apolipoprotein E knockout mice.

Xin Guo, Sohsuke Yamada, Akihide Tanimoto, Yan Ding, Ke-Yong Wang, Shohei Shimajiri, Yoshitaka Murata, Satoshi Kimura, Takashi Tasaki, Atsunori Nabeshima and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 73 citations in OpenAlex.

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  11. Sex-Biased Gene Expression ofEvidence-based complementary and alternative medicine : eCAM · 2021
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  16. Protective Effects of Peroxiredoxin 4 (PRDX4) on Cholestatic Liver Injury.International journal of molecular sciences · 2018
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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

13 authors at 5 institutions in 2 countries.

Xin GuoDepartment of Pathology and Cell Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Sohsuke Yamada
Akihide Tanimoto
Yan Ding
Ke-Yong Wang
Shohei Shimajiri
Yoshitaka Murata
Satoshi Kimura
Takashi Tasaki
Atsunori Nabeshima
Teruo Watanabe
Kimitoshi Kohno
Yasuyuki Sasaguri
University of Occupational and Environmental Health Japan · JPHebei Medical University · CNKagoshima University · JPKyushu Institute of Technology · JPUji Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimA growing body of evidence has shown that increased formation of oxidized molecules and reactive oxygen species within the vasculature (i.e., the extracellular space) plays a crucial role in the initiation and progression of atherosclerosis and in the formation of unstable plaques. Peroxiredoxin 4 (PRDX4) is the only known secretory member of the antioxidant PRDX family. However, the relationship between PRDX4 and susceptibility to atherosclerosis has remained unclear.

resultsTo define the role of PRDX4 in hyperlipidemia-induced atherosclerosis, we generated hPRDX4 transgenic (Tg) and apolipoprotein E (apoE) knockout mice (hPRDX4(+/+)/apoE(-/-)). After feeding the mice a high-cholesterol diet, they showed fewer atheromatous plaques, less T-lymphocyte infiltration, lower levels of oxidative stress markers, less necrosis, a larger number of smooth muscle cells, and a larger amount of collagen, resulting in thickened fibrous cap formation and possible stable plaque phenotype as compared with apoE(-/-) mice. We also detected greater suppression of apoptosis and decreased Bax expression in hPRDX4(+/+)/apoE(-/-) mice than in apoE(-/-) mice. Bone marrow transplantation from hPRDX4(+/+) donors to apoE(-/-) mice confirmed the antiatherogenic aspects of PRDX4, revealing significantly suppressed atherosclerotic progression. INNOVATION: In this study, we demonstrated for the first time that PRDX4 suppressed the development of atherosclerosis in apoE(-/-) mice fed a high-cholesterol diet.

conclusionThese data indicate that PRDX4 is an antiatherogenic factor and, by suppressing oxidative damage and apoptosis, that it may protect against the formation of vulnerable (unstable) plaques.

Indexed as

AnimalsApolipoproteins EAtherosclerosisBlotting, WesternEnzyme-Linked Immunosorbent AssayImmunohistochemistryMaleMiceMice, KnockoutMice, TransgenicOxidative StressPeroxiredoxinsReactive Oxygen SpeciesApolipoproteins EPeroxiredoxinsReactive Oxygen Species

Identifiers

PMID22548251
PMCPMC3437049
OpenAlexW1991638553

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.