Evidence map›Paper›PMID 38910326›Full record

ReviewMolecular therapy : the journal of the American Society of Gene Therapy2024

Preclinical evidence in the assembly of mammalian SWI/SNF complexes: Epigenetic insights and clinical perspectives in human lung disease therapy.

Octavio A Trejo-Villegas, Irene H Heijink, Federico Ávila-Moreno

Abstract readReview
In one paragraph

Review in Molecular therapy : the journal of the American Society of Gene Therapy, 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. Review
  3. Article
  4. RNA and epigenetic editing: The new frontier in gene and cell therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. 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

3 authors.

Octavio A Trejo-VillegasLung Diseases and Functional Epigenomics Laboratory (LUDIFE), Biomedicine Research Unit (UBIMED), Facultad de Estudios Superiores-Iztacala (FES-Iztacala), Universidad Nacional Autónoma de México (UNAM), Avenida de los Barrios #1, Colonia Los Reyes Iztacala, Tlalnepantla de Baz, 54090, Estado de México, México.
Irene H HeijinkDepartments of Pathology & Medical Biology and Pulmonology, GRIAC Research Institute, University Medical Center Groningen, University of Groningen, 9713 Groningen, the Netherlands.
Federico Ávila-MorenoLung Diseases and Functional Epigenomics Laboratory (LUDIFE), Biomedicine Research Unit (UBIMED), Facultad de Estudios Superiores-Iztacala (FES-Iztacala), Universidad Nacional Autónoma de México (UNAM), Avenida de los Barrios #1, Colonia Los Reyes Iztacala, Tlalnepantla de Baz, 54090, Estado de México, México; Research Unit, Instituto Nacional de Enfermedades Respiratorias (INER), Ismael Cosío Villegas, 14080, Ciudad de México, México; Research Tower, Subdirección de Investigación Básica, Instituto Nacional de Cancerología (INCan), 14080, Ciudad de México, México. Electronic address: f.avila@unam.mx.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SWI/SNF complex, also known as the BRG1/BRM-associated factor (BAF) complex, represents a critical regulator of chromatin remodeling mechanisms in mammals. It is alternatively referred to as mSWI/SNF and has been suggested to be imbalanced in human disease compared with human health. Three types of BAF assemblies associated with it have been described, including (1) canonical BAF (cBAF), (2) polybromo-associated BAF (PBAF), and (3) non-canonical BAF (ncBAF) complexes. Each of these BAF assemblies plays a role, either functional or dysfunctional, in governing gene expression patterns, cellular processes, epigenetic mechanisms, and biological processes. Recent evidence increasingly links the dysregulation of mSWI/SNF complexes to various human non-malignant lung chronic disorders and lung malignant diseases. This review aims to provide a comprehensive general state-of-the-art and a profound examination of the current understanding of mSWI/SNF assembly processes, as well as the structural and functional organization of mSWI/SNF complexes and their subunits. In addition, it explores their intricate functional connections with potentially dysregulated transcription factors, placing particular emphasis on molecular and cellular pathogenic processes in lung diseases. These processes are reflected in human epigenome aberrations that impact clinical and therapeutic levels, suggesting novel perspectives on the diagnosis and molecular therapies for human respiratory diseases.

Indexed as

Chromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneEpigenesis, GeneticLung DiseasesTranscription FactorsAnimalsDNA HelicasesGene Expression RegulationHumansNuclear ProteinsChromosomal Proteins, Non-HistoneDNA HelicasesNuclear ProteinsSMARCA4 protein, humanSWI-SNF-B chromatin-remodeling complexTranscription FactorscancercBAFlungmSWI/SNFncBAFPBAFtherapy

Identifiers

PMID38910326
PMCPMC11405180

What OpenQuestion holds

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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.