Evidence map›Paper›PMID 35743055›Full record

ReviewInternational journal of molecular sciences2022

Role of MicroRNAs in Signaling Pathways Associated with the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Focus on Epithelial-Mesenchymal Transition.

Ana Ruth Cadena-Suárez, Hilda Arely Hernández-Hernández, Noé Alvarado-Vásquez, Claudia Rangel-Escareño, Bettina Sommer, María Cristina Negrete-García

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Examining the contribution of Notch signaling to lung disease development.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  5. Review
  6. When a DEAD-Box Protein Is the Key: A Novel Role for DDX5 in Lung Pericyte Dysfunction.American journal of respiratory cell and molecular biology · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Observational
  17. Short histological kaleidoscope - recent findings in histology. Part III.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

6 authors at 2 institutions in 1 country.

Ana Ruth Cadena-SuárezLaboratorio de Biología Molecular, Instituto Nacional de Enfermedades Respiratorias (INER) "Ismael Cosío Villegas", Calz. Tlalpan 4502, Col. Sección XVI, Mexico City 14080, Mexico.
Hilda Arely Hernández-HernándezLaboratorio de Biología Molecular, Instituto Nacional de Enfermedades Respiratorias (INER) "Ismael Cosío Villegas", Calz. Tlalpan 4502, Col. Sección XVI, Mexico City 14080, Mexico.
Noé Alvarado-VásquezDepartamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias (INER) "Ismael Cosío Villegas", Calz. Tlalpan 4502, Col. Sección XVI, Mexico City 14080, Mexico.
Claudia Rangel-EscareñoDepartamento de Genomica Computacional, Instituto Nacional de Medicina Genómica, Periférico Sur 4809, Col. Arenal Tepepan, Mexico City 14610, Mexico.
Bettina SommerDepartamento de Investigación en Hiperreactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias (INER) "Ismael Cosío Villegas", Calz. Tlalpan 4502, Col. Sección XVI, Mexico City 14080, Mexico.ORCID 0000-0003-1292-9418
María Cristina Negrete-GarcíaLaboratorio de Biología Molecular, Instituto Nacional de Enfermedades Respiratorias (INER) "Ismael Cosío Villegas", Calz. Tlalpan 4502, Col. Sección XVI, Mexico City 14080, Mexico.ORCID 0000-0002-8264-0858
Instituto Nacional de Enfermedades Respiratorias · MXNational Institute of Genomic Medicine · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive disease with high mortality and unclear etiology. Previous evidence supports that the origin of this disease is associated with epigenetic alterations, age, and environmental factors. IPF initiates with chronic epithelial lung injuries, followed by basal membrane destruction, which promotes the activation of myofibroblasts and excessive synthesis of extracellular matrix (ECM) proteins, as well as epithelial-mesenchymal transition (EMT). Due to miRNAs' role as regulators of apoptosis, proliferation, differentiation, and cell-cell interaction processes, some studies have involved miRNAs in the biogenesis and progression of IPF. In this context, the analysis and discussion of the probable association of miRNAs with the signaling pathways involved in the development of IPF would improve our knowledge of the associated molecular mechanisms, thereby facilitating its evaluation as a therapeutic target for this severe lung disease. In this work, the most recent publications evaluating the role of miRNAs as regulators or activators of signal pathways associated with the pathogenesis of IPF were analyzed. The search in Pubmed was made using the following terms: "miRNAs and idiopathic pulmonary fibrosis (IPF)"; "miRNAs and IPF and signaling pathways (SP)"; and "miRNAs and IPF and SP and IPF pathogenesis". Additionally, we focus mainly on those works where the signaling pathways involved with EMT, fibroblast differentiation, and synthesis of ECM components were assessed. Finally, the importance and significance of miRNAs as potential therapeutic or diagnostic tools for the treatment of IPF are discussed.

Indexed as

Idiopathic Pulmonary FibrosisMicroRNAsEpithelial-Mesenchymal TransitionHumansMyofibroblastsSignal TransductionMicroRNAsEMTidiopathic pulmonary fibrosismiRNAsmyofibroblasts

Identifiers

PMID35743055
PMCPMC9224458
OpenAlexW4282934440

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.