Evidence map›Paper›PMID 34292473›Full record

ArticleMolecular biology reports2021

Relationship of endoplasmic reticulum stress with the etiopathogenesis of chronic tonsillitis and tonsillar hypertrophy in pediatric patients: a prospective, parallel-group study.

Merih Onal, Nadir Kocak, Fahrettin Duymus, Mete Kaan Bozkurt, Cagdas Elsurer, Omer Erdur, Ozkan Onal

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04653376 (Possible Relationship Between Apoptosis and Endoplasmic Reticulum Stress in the Etiopathogenesis of Chronic Tonsillitis and Tonsillar Hypertrophy), which is not on this map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 34% 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.

NCT04653376 completednot on this map

Possible Relationship Between Apoptosis and Endoplasmic Reticulum Stress in the Etiopathogenesis of Chronic Tonsillitis and Tonsillar Hypertrophy

TypeobservationalSponsorSelcuk UniversityRan2018 to 2019Enrolled46ConditionsTonsillitis, Tonsillar Hypertrophy, Immune System DiseasesArmsTonsillectomy surgery
3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
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 2 institutions in 2 countries.

Merih OnalDepartment of Otolaryngology, Faculty of Medicine, Selcuk University, Konya, Turkey. drmerihonal@gmail.com.ORCID http://orcid.org/0000-0003-0591-8411
Nadir KocakDepartment of Medical Genetics, Faculty of Medicine, Selcuk University, Konya, Turkey.ORCID https://orcid.org/0000-0002-1727-1582
Fahrettin DuymusDepartment of Medical Genetics, Faculty of Medicine, Selcuk University, Konya, Turkey.ORCID https://orcid.org/0000-0002-8130-9792
Mete Kaan BozkurtDepartment of Otolaryngology, Faculty of Medicine, Selcuk University, Konya, Turkey.ORCID https://orcid.org/0000-0002-3153-3294
Cagdas ElsurerDepartment of Otolaryngology, Faculty of Medicine, Selcuk University, Konya, Turkey.ORCID https://orcid.org/0000-0001-9804-7023
Omer ErdurDepartment of Otolaryngology, Faculty of Medicine, Selcuk University, Konya, Turkey.ORCID https://orcid.org/0000-0002-5596-0100
Ozkan OnalDepartment of Outcomes Research, Cleveland Clinic Anesthesiology Institute, Cleveland, OH, USA.ORCID https://orcid.org/0000-0002-5574-1901
Selçuk University · TRCleveland Clinic · US

Funding

Selçuk Üniversitesi 19401029
6 · The paper itself

Abstract

objectivesTonsil tissue is a very important component of the human immunity system, contributing to the functioning of the cellular and humoral defence system, especially in childhood. The endoplasmic reticulum (ER) is an organelle that has a very important function in the balanced functioning of cells, in which the accumulation of a cellular protein called ER stress occurs in case of dysfunction. ER stress influences the pathogenesis of many diseases and immune system functions. We aimed to investigate the relation between the diseases of tonsil tissue and ER stress response to elucidate the mechanisms of diseases related with the immune system.

methodsA prospective study was conducted in 46 children aged between 2 and 16 years who underwent tonsillectomy for chronic tonsillitis or tonsillar hypertrophy. Tonsil tissue was separated into two groups according to their size and evaluated in terms of ER stress markers and apoptosis markers by Real-time PCR and Western blot analysis.

resultsThe ΔCT levels of ER stress markers (ATF4, ATF6, CHOP, GRP78, EIF2AK3, ERN1, GRP94) were greater in children with chronic tonsillitis (p < 0.005). In contrast, the tonsillar hypertrophy group had greater ΔCT levels of apoptosis markers (BAX, BCL-2) according to the Real-time PCR method (p < 0.005). According to the Western blot analysis, the normalized levels of ATF4, ATF6, CHOP, GRP78, and ERN1 genes were found greater in the chronic tonsillitis group than the tonsillar hypertrophy group. There was no difference between the two groups in terms of normalized BCL-2 and BAX levels by Western blot analysis.

conclusionThis is the first study in the literature investigating the effect of the ER stress pathway on the etiopathogenesis of tonsil diseases. It was concluded that the ER stress pathway plays a role in the etiopathogenesis of chronic tonsillitis. Investigating the relationship between ER stress and structures such as the tonsil tissue that make up the immune system can help create new treatment strategies. CLINICAL

trial registrationTrial Registration ClinicalTrials.gov Identifier: NCT04653376.

Indexed as

Disease SusceptibilityEndoplasmic Reticulum StressAdolescentApoptosisBiomarkersChildChild, PreschoolChronic DiseaseFemaleHumansHypertrophyMalePalatine TonsilReal-Time Polymerase Chain ReactionTonsillitisBiomarkersApoptosisChildrenEndoplasmic reticulum stressGeneticsPalatine tonsilTonsillitis

Identifiers

PMID34292473
OpenAlexW3158936036

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.