Evidence map›Paper›PMID 26801626›Full record

ArticleLipids in health and disease2016

Early-stage atherosclerosis in poloxamer 407-induced hyperlipidemic mice: pathological features and changes in the lipid composition of serum lipoprotein fractions and subfractions.

Tatyana A Korolenko, Thomas P Johnston, Fedor V Tuzikov, Natalia A Tuzikova, Alexandr B Pupyshev, Victor K Spiridonov, Natalya V Goncharova, Igor V Maiborodin, Natalia A Zhukova

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 34 citations in OpenAlex.

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  9. Differential expression of full-length and NHAmerican journal of physiology. Gastrointestinal and liver physiology · 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

9 authors at 6 institutions in 2 countries.

Tatyana A KorolenkoInstitute of Physiology and Fundamental Medicine, Siberian Branch of the Russian Academy of Medical Sciences, Timakov St. 4, Novosibirsk, 630117, Russia. t.a.korolenko@physiol.ru.
Thomas P JohnstonDivision of Pharmaceutical Sciences, School of Pharmacy, University of Missouri-Kansas City, Rm. 4243, HSB, 2464 Charlotte Street, Kansas City, MO, 64108-2718, USA. johnstont@umkc.edu.
Fedor V TuzikovBoreskov Institute of Catalysis, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia. tuzikov@catalysis.ru.
Natalia A TuzikovaBoreskov Institute of Catalysis, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia. tuzikova@catalysis.ru.
Alexandr B PupyshevNovosibirsk State Medical University, Novosibirsk, Russia. apupyshev@mail.ru.
Victor K SpiridonovInstitute of Physiology and Fundamental Medicine, Siberian Branch of the Russian Academy of Medical Sciences, Timakov St. 4, Novosibirsk, 630117, Russia.
Natalya V GoncharovaInstitute of Physiology and Fundamental Medicine, Siberian Branch of the Russian Academy of Medical Sciences, Timakov St. 4, Novosibirsk, 630117, Russia. natalya15.ru@rambler.ru.
Igor V MaiborodinSiberian Division of the Russian Academy of Sciences, Institute of Chemical Biology and Basic Medicine, Novosibirsk, Russia. imai@mail.ru.
Natalia A ZhukovaVorozhtzov N.N. Institute of Organic Chemistry, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia. GNA2004@ngs.ru.
Research Institute of Physiology and Fundamental Medicine of the Siberian Branch of the Russian Academy of Medical Sciences · RUBoreskov Institute of Catalysis · RUNovosibirsk Institute of Organic Chemistry · RUNovosibirsk State Medical University · RUSiberian Branch of the Russian Academy of Sciences · RUUniversity of Missouri–Kansas City · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aims of this study were to evaluate the effect of poloxamer 407 administration on atherogenic serum lipoprotein fractions and subfractions associated with cholesterol, triglycerides and phospholipids, as well as the onset of early atherosclerosis, in mice.

methodsMice were administered either sterile saline or poloxamer 407 (to induce a dose-controlled hyperlipidemia) for 1 month and then sacrificed at 1, 4 and 10 days after the last dose of poloxamer 407. Systolic and diastolic blood pressure, the activity of a cysteine protease (cathepsin B) in cardiac and liver tissue, and histological/morphological examination of heart and liver specimens was performed for each group of mice at each time point. Lastly, small angle X-ray scattering was utilized to analyze the lipoprotein fractions and subfractions associated with cholesterol, triglycerides and phospholipids for both groups of mice at each time point. Statistical analysis was performed using one-way, analysis-of-variance with post hoc analysis to determine significantly different mean values, while correlation analysis employed the Spearman test.

resultsPoloxamer 407-treated mice revealed significant hyperlipidemia, moderately elevated blood pressure, general lipidosis in liver cells, increased cysteine protease activity in heart tissue, and contractile-type changes in cardiomyocytes. Similar to humans, the onset of atherosclerosis in poloxamer 407-treated mice was characterized by a steady increase in serum low-density, intermediate-density and very-low-density lipoprotein fractions, as well as very-low-density lipoprotein subfractions.

conclusionsWe would propose that the sustained elevation of serum atherogenic lipoprotein fractions and subfractions induced by the administration of poloxamer 407 to mice resulted in the morphological changes we observed in both heart and liver cells, which are suggested to precede atherosclerosis, since this is a well-established mouse model of atherosclerosis. Since most of the cellular, biochemical and physiological changes documented in the present study using poloxamer 407-treated mice are related to the symptoms of early atherosclerosis in humans, it is suggested that the poloxamer 407-induced mouse model of hyperlipidemia and atherosclerosis might prove beneficial as an experimental animal model with which to evaluate the pathological features observed in early-stage atherosclerosis.

Indexed as

Alanine TransaminaseAnimalsAspartate AminotransferasesAtherosclerosisBlood GlucoseBlood PressureCathepsin BDiastoleHyperlipidemiasIntracellular MembranesLipoproteinsLiverLysosomesMaleMice, Inbred CBAMyocardiumAlanine TransaminaseAspartate AminotransferasesBlood GlucoseCathepsin BLipoproteinsPoloxamer

Identifiers

PMID26801626
PMCPMC4724105
OpenAlexW2257996152

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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.