Evidence map›Paper›PMID 39795977›Full record

ReviewInternational journal of molecular sciences2024

The Molecular Basis of Asthma Exacerbations Triggered by Viral Infections: The Role of Specific miRNAs.

Natalia Kierbiedź-Guzik, Barbara Sozańska

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. 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

2 authors.

Natalia Kierbiedź-GuzikDepartment and Clinic of Paediatrics, Allergology and Cardiology, Wroclaw Medical University, ul. Chałubińskiego 2a, 50-368 Wrocław, Poland.
Barbara SozańskaDepartment and Clinic of Paediatrics, Allergology and Cardiology, Wroclaw Medical University, ul. Chałubińskiego 2a, 50-368 Wrocław, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viral respiratory infections are a significant clinical problem among the pediatric population and are one of the leading causes of hospitalization. Most often, upper respiratory tract infections are self-limiting. Still, those that involve the lower respiratory tract are usually associated with asthma exacerbations, leading to worsening or even the initiation of the disease. A key role in regulating the immune response and inflammation during viral infections and their impact on the progression of asthma has been demonstrated for miRNA molecules (microRNA). Their interaction with mRNA (messenger RNA) regulates gene expression in innate and acquired immune responses, making them valuable biomarkers for diagnostics, monitoring, and predicting asthma exacerbations. The following paper presents changes in the expression of miRNAs during the five most common viral infections causing asthma worsening, with particular emphasis on the pediatric population. In addition, we describe the molecular mechanisms by which miRNAs influence the pathogenesis of viral infection, immune responses, and asthma exacerbations. These molecules represent promising targets for future innovative therapeutic strategies, paving the way for developing personalized medicine for patients with viral-induced asthma exacerbations.

Indexed as

AsthmaMicroRNAsRespiratory Tract InfectionsVirus DiseasesBiomarkersDisease ProgressionGene Expression RegulationHumansBiomarkersMicroRNAsasthmabiomarkerschildrenexacerbationinfluenza virusmetapneumovirusmiRNArespiratory syncytial virusrhinovirusSevere Acute Respiratory Syndrome Coronavirus 2

Identifiers

PMID39795977
PMCPMC11720134

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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.