Evidence map›Paper›PMID 34308503›Full record

ArticleHeart and vessels2021

Oxidative stress-responsive apoptosis-inducing protein in patients with heterozygous familial hypercholesterolemia.

Kayoko Sato, Takako Yao, Tsutomu Fujimura, Kimie Murayama, Ko Okumura, Nobuhisa Hagiwara, Yoshinori Seko

Abstract read
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In one paragraph

Article in Heart and vessels, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 7 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 4 institutions in 1 country.

Kayoko SatoDepartment of Cardiology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan. sato.kayoko@twmu.ac.jp.ORCID http://orcid.org/0000-0001-8694-7155
Takako YaoDivision of Cardiovascular Medicine, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.
Tsutomu FujimuraLaboratory of Bioanalytical Chemistry, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
Kimie MurayamaDivision of Proteomics and Biomolecular Science, Graduate School of Medicine, BioMedical Research Center, Juntendo University, Tokyo, Japan.
Ko OkumuraDepartment of Biofunctional Microbiota, School of Medicine, Juntendo University, Tokyo, Japan.
Nobuhisa HagiwaraDepartment of Cardiology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Yoshinori SekoDepartment of Biofunctional Microbiota, School of Medicine, Juntendo University, Tokyo, Japan.
Juntendo University · JPTokyo Women's Medical University · JPThe Institute of Medical Science, Asahi Life Foundation · JPTohoku Medical and Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress, an inducer of apoptosis, plays a critical role in ischemia/reperfusion injury and atherosclerosis. We previously identified an apoptosis-inducing ligand, the post-translationally modified secreted form of eukaryotic translation initiation factor 5A (eIF5A), 'oxidative stress-responsive apoptosis-inducing protein' (ORAIP). In this study, we investigated the role of ORAIP in patients with heterozygous familial hypercholesterolemia (HeFH), a leading cause of premature cardiovascular disease. We analyzed plasma ORAIP and oxidized low-density lipoprotein (oxLDL) levels in 60 patients with HeFH (60% male, 57.0 ± 13.6 years of age) and 20 patients with LDL-C hypercholesterolemia (DL, 85% male, 64.1 ± 13.3 years of age). The coronary artery atherosclerosis from the patients with HeFH who had a coronary artery bypass graft was investigated by double immunostaining. The plasma ORAIP levels in the patients with HeFH were significantly elevated compared to those in the patients with DL (73.5 ± 46.0 vs. 48.3 ± 21.4 ng/mL, p = 0.0277). The plasma oxLDL levels in HeFH patients were also elevated (156.8 ± 65.2 vs. 123.7 ± 46.6 mg/dL, p = 0.0461) compared to those in DL patients and correlated with maxLDL-C levels (R = 0.4454, p = 0.00648). Double-immunostaining of ORAIP and oxLDL in the coronary artery from patients with HeFH who had a coronary artery bypass graft showed that ORAIP and oxLDL were colocalized with apoptotic vascular smooth muscle cells in the atherosclerotic plaque. ORAIP plays a role in the development of oxidative stress-induced atherosclerosis and may be an important therapeutic target for plaque rupture in patients with HeFH.

Indexed as

Hyperlipoproteinemia Type IIAdultAgedApoptosisApoptosis Regulatory ProteinsAtherosclerosisFemaleHumansHypercholesterolemiaMaleMiddle AgedOxidative StressPlaque, AtheroscleroticApoptosis Regulatory ProteinsAtherosclerosisCoronary artery diseaseHeterozygous familial hypercholesterolemiaOxidative stress-responsive proteinPlaque rupture

Identifiers

PMID34308503
OpenAlexW3184823543

What OpenQuestion holds

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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.