Evidence map›Paper›PMID 34025671›Full record

ReviewFrontiers in immunology2021

Implications the Role of miR-155 in the Pathogenesis of Autoimmune Diseases.

Salar Pashangzadeh, Morteza Motallebnezhad, Fatemeh Vafashoar, Azadeh Khalvandi, Nazanin Mojtabavi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

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  16. Knockdown of miR-155 alleviates skin damage in rats with chronic spontaneous urticaria by modulating the JAK/STAT signaling pathway.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024
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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 1 institution in 1 country.

Salar PashangzadehDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Morteza MotallebnezhadDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Fatemeh VafashoarDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Azadeh KhalvandiDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Nazanin MojtabaviDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Iran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small noncoding conserved RNAs containing 19 to 24 nucleotides that are regulators of post-translational modifications and are involved in the majority of biological processes such as immune homeostasis, T helper cell differentiation, central and peripheral tolerance, and immune cell development. Autoimmune diseases are characterized by immune system dysregulation, which ultimately leads to destructive responses to self-antigens. A large body of literature suggests that autoimmune diseases and immune dysregulation are associated with different miRNA expression changes in the target cells and tissues of adaptive or innate immunity. miR-155 is identified as a critical modulator of immune responses. Recently conducted studies on the expression profile of miR-155 suggest that the altered expression and function of miR-155 can mediate vulnerability to autoimmune diseases and cause significant dysfunction of the immune system.

Indexed as

AutoimmunityImmune ToleranceAnimalsAutoimmune DiseasesGene Expression RegulationHumansMicroRNAsSignal TransductionMicroRNAsMIRN155 microRNA, humanautoimmune diseaseimmune systemmiR-155miRNAtolerance

Identifiers

PMID34025671
PMCPMC8137895
OpenAlexW3162535811

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.