Evidence map›Paper›PMID 39166676›Full record

ArticleRevista da Associacao Medica Brasileira (1992)2024

Contributing role of metabolic genes APOE, FTO, and LPL in the development of atrial fibrillation: insights from a case-control study.

Saira Rafaqat, Saima Sharif, Shagufta Naz, Dimitrios Patoulias, Aleksandra Klisic

Abstract read
In one paragraph

Article in Revista da Associacao Medica Brasileira (1992), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

2 citing papers in PubMed.

  1. Review
  2. FTO in health and disease.Frontiers in cell and developmental biology · 2024
    Review
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.

Saira RafaqatLahore College for Women University, Department of Zoology - Lahore, Pakistan.ORCID http://orcid.org/0000-0001-7177-5602
Saima SharifLahore College for Women University, Department of Zoology - Lahore, Pakistan.ORCID http://orcid.org/0000-0003-3169-2380
Shagufta NazLahore College for Women University, Department of Zoology - Lahore, Pakistan.ORCID http://orcid.org/0000-0001-9699-5193
Dimitrios PatouliasAristotle University of Thessaloniki, General Hospital "Hippokration", Second Department of Cardiology, Outpatient Department of Cardiometabolic Medicine - Thessaloniki, Greece.ORCID http://orcid.org/0000-0002-6899-684X
Aleksandra KlisicUniversity of Montenegro, Faculty of Medicine - Podgorica, Montenegro.ORCID http://orcid.org/0000-0001-7870-0996

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of the study was to examine the expression profile of genes (APOE, FTO, and LPL) associated with metabolic syndrome (MetS) in subjects with concomitant atrial fibrillation (AF).

methodsA total of 690 subjects were categorized into control, AF without MetS, and AF with MetS.

resultsThe expression profiles of the APOE, FTO, and LPL genes were decreased in AF subjects and AF subjects with MetS as compared to the controls. In AF without the MetS group, an inverse relationship was found between the expression of the LPL gene with body mass index (BMI) and a positive relationship with creatine kinase-MB, whereas expression of the FTO gene was inversely associated with fasting blood glucose and positively with cardiac troponin I in AF suffering from MetS. Expression of the LPL gene was directly linked with systolic blood pressure (SBP) and high-density lipoprotein-cholesterol (HDL-C), whereas an inverse correlation with heart rate and expression of the FTO gene in AF with MetS were shown. The expression of the LPL gene was inversely related to BMI in subjects with AF. The expression of the LPL gene was positively correlated with SBP and HDL-C and negatively correlated with heart rate, while the expression of the FTO gene was an important predictor of AF with MetS.

conclusionThe decreased expression of APOE, FTO, and LPL genes in AF with and without MetS indicates their potential contributing role in the pathogenesis of AF.

Indexed as

Alpha-Ketoglutarate-Dependent Dioxygenase FTOApolipoproteins EAtrial FibrillationBody Mass IndexLipoprotein LipaseMetabolic SyndromeAgedBlood GlucoseBlood PressureCase-Control StudiesCholesterol, HDLFemaleHumansMaleMiddle AgedAlpha-Ketoglutarate-Dependent Dioxygenase FTOApolipoproteins EBlood GlucoseCholesterol, HDLFTO protein, humanLipoprotein Lipase

Identifiers

PMID39166676
PMCPMC11329263

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