Evidence map›Paper›PMID 26670457›Full record

ArticleJournal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing2016

Heat shock protein 70 gene polymorphisms' influence on the electrophysiology of long QT syndrome.

Altaf Ali, Sameera F Qureshi, Veronica Medikare, Ananthapur Venkateshwari, Narsimhan Calambur, Hygriv Rao, M P Jayakrishnan, Jayaprakash Shenthar, Kumarasamy Thangaraj, Pratibha Nallari

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In one paragraph

Article in Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing, 2016. 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
0.5field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

10 authors at 6 institutions in 1 country.

Altaf AliDepartment of Genetics, University College of Science, Osmania University, Hyderabad, Telangana, 500007, India.
Sameera F QureshiDepartment of Genetics, University College of Science, Osmania University, Hyderabad, Telangana, 500007, India.
Veronica MedikareDepartment of Genetics, University College of Science, Osmania University, Hyderabad, Telangana, 500007, India.
Ananthapur VenkateshwariInstitute of Genetics and Hospital for Genetic Diseases, Osmania University, Begumpet, Hyderabad, Telangana, 500016, India.
Narsimhan CalamburCare Hospital, Hyderabad, Telangana, India.
Hygriv RaoKrishna Institute of Medical Sciences, 1-8-31/1, Minister Road, Secunderabad, Telangana, 500 003, India.
M P JayakrishnanInstitute of Maternal and Child Health, Calicut Medical College, Calicut 8, Kerala, India.
Jayaprakash ShentharSri Jayadeva Institute of Cardiovascular Science and Research, Jayanagar 9th Block, Bannerghatta Road, Bangalore, Karnataka, 560069, India.
Kumarasamy ThangarajCentre for Cellular and Molecular Biology, Uppal Road, Hyderabad, Telangana, 500 007, India.
Pratibha NallariDepartment of Genetics, University College of Science, Osmania University, Hyderabad, Telangana, 500007, India. prathinallari@yahoo.com.
Osmania University · INCARE Hospitals · INCentre for Cellular and Molecular Biology · INGovernment Medical College · INKrishna Institute of Medical Sciences · INSri Jayadeva Institute of Cardiovascular Sciences and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLong QT syndrome (LQTS) is a rare cardiac disorder caused due to mutations in genes encoding ion channels responsible for generation of electrical impulses. The heat shock protein (HSP)-70 gene, expressed under conditions of stress, plays a cardioprotective role when overexpressed and helps in the proper folding of the nascent proteins synthesized by the cellular machinery. We aimed to identify the role played by HSP-70 gene polymorphisms in the pathogenesis of LQTS.

methodsStudy included 49 LQTS patients, 71 family members, and 219 healthy individuals recruited from an ethnically matched population. Genotyping of the single-nucleotide polymorphisms (SNPs) rs1043618 (HSP-70-1, +190G/C), rs1061581 (HSP-70-2, +1267A/G), and rs2227956 (HSP-70-hom, +2437T/C) was performed by PCR-RFLP analysis, and the results were analyzed statistically at 95 % confidence interval and p ≤ 0. 05.

resultsThe "C" allele of HSP-70-1 (+190G/C) and "G" allele of HSP-70-2 (+1267A/G) showed strong association with LQTS phenotype. The haplotype group C-G-T consisting of two risk alleles was significantly associated with the disease condition. Multifactor dimensionality reduction analysis further substantiated that the three-allele model influences the outcome of the phenotype highlighting the effect of modifiers in the etiology of LQTS.

conclusionsAs HSP-70 influences the channel assembly and maturation/trafficking of the ion channel proteins, the alleles C of the HSP-70-1 and G of the HSP-70-2 loci and the haplotype group C-G-T could be considered a diagnostic biomarker in the identification of the LQTS phenotype with a potential to affect the progression and modification of the disease phenotype.

Indexed as

AdultAge DistributionFemaleGenetic MarkersGenetic Predisposition to DiseaseHSP70 Heat-Shock ProteinsHumansIndiaLong QT SyndromeMalePolymorphism, Single NucleotidePrevalenceRisk FactorsSex DistributionGenetic MarkersHSP70 Heat-Shock ProteinsElectrophysiologyHaplotypeHSP-70Long QT syndromeProtein foldingSNP

Identifiers

PMID26670457
OpenAlexW2297989178

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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.