Evidence map›Paper›PMID 34418957›Full record

ArticleBMC cardiovascular disorders2021

Abnormalities in lysine degradation are involved in early cardiomyocyte hypertrophy development in pressure-overloaded rats.

Jialing Liu, Junhao Hu, Lanlan Tan, Qi Zhou, Xiaojing Wu

Open access · goldAbstract read
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Article in BMC cardiovascular disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 15 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

5 authors at 2 institutions in 1 country.

Jialing LiuCardiovascular Department of the Second Affiliated Hospital of Chongqing Medical University, NO.74 Linjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China.
Junhao HuCardiovascular Department of the Second Affiliated Hospital of Chongqing Medical University, NO.74 Linjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China.
Lanlan TanCardiovascular Department of the Second Affiliated Hospital of Chongqing Medical University, NO.74 Linjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China.
Qi ZhouCardiovascular Department of the Second Affiliated Hospital of Chongqing Medical University, NO.74 Linjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China. drzhouqi@126.com.
Xiaojing WuCardiovascular Department of Shenzhen University General Hospital and Shenzhen University Clinical Medical Academy, NO.1098 Xueyuan Street, Nanshan District, Shenzhen, 518060, People's Republic of China. xiaojingwu1992@163.com.ORCID 0000-0002-0590-7627
Dalian Medical University · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiomyocyte metabolism changes before cardiac remodeling, but its role in early cardiac hypertrophy detection remains unclear. This study investigated early changes in plasma metabolomics in a pressure-overload cardiac hypertrophy model induced by transverse aortic constriction (TAC).

methodsThe TAC model was constructed by partly ligating the aortic arch. Twelve Sprague-Dawley rats were randomly divided into the TAC group (n = 6) and sham group (n = 6). Three weeks after surgery, cardiac echocardiography was performed to assess cardiac remodeling and function. Hematoxylin/eosin (HE), Masson, and wheat germ agglutinin (WGA) stains were used to observe pathological changes. Plasma metabolites were detected by UPLC-QTOFMS and Q-TOFMS. Specific metabolites were screened by orthogonal partial least squares discriminant analysis (OPLS-DA). Metabolic pathways were characterized by Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and the predictive value of the screened metabolites was analyzed by receiver operating characteristic (ROC) curve analysis.

resultsThree weeks after surgery, the TAC and sham groups had similar left heart function and interventricular septum and diastolic left ventricular posterior wall thicknesses. However, on pathological examination, the cross-sectional area of cardiomyocytes and myocardial fibrosis severity were significantly elevated in TAC rats. OPLS-DA showed different metabolic patterns between the TAC and sham groups. Based on the criteria VIP > 1 and P < 0.05, 13 metabolites were screened out. KEGG analysis identified disrupted lysine degradation through the related metabolites 5-aminopentanoic acid, N6-acetyl-L-lysine, and L-lysine, with areas under the ROC curve (AUCs) of 0.917, 0.889, and 0.806, respectively, for predicting compensated cardiomyocyte hypertrophy.

conclusionDisruption of lysine degradation might be involved in early cardiac hypertrophy development, and related metabolites might be potential predictive and interventional targets for subclinical cardiomyocyte hypertrophy.

Indexed as

Energy MetabolismVentricular Function, LeftVentricular RemodelingAnimalsAorta, ThoracicArterial PressureDisease Models, AnimalFibrosisHypertrophy, Left VentricularLigationLysineMaleMetabolomeMetabolomicsMyocardiumProteolysisLysineCardiac hypertrophyLysine degradationMetabolomicsNonenergetic metabolismPressure overload

Identifiers

PMID34418957
PMCPMC8379758
OpenAlexW3195151002

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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.