ArticleRedox biology2023
Myosin light-chain 4 gene-transfer attenuates atrial fibrosis while correcting autophagic flux dysregulation.
Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Altitude-Related Adaptation in Freshwater Snails (Animals : an open access journal from MDPI · 2026Article
- Human iPSCs: atrial versus ventricular cardiomyocytes and their functional and pharmacological differences.Biochemical Society transactions · 2026Review
- Association of radiotherapy with atrial fibrillation-related gene expression in breast cancer patients: a study based on the TCGA-BRCA database.Discover oncology · 2026Article
- Genome-wide association study of myopia progression in Chinese adolescents and application of polygenic risk score prediction.Frontiers in chemistry · 2026Article
- Gene Therapy for Inherited Cardiac Arrhythmias.Journal of cardiovascular translational research · 2025Review
- Identification and validation of parthanatos-related genes in end-stage renal disease.Renal failure · 2025Article
- An Insect Salivary Sheath Protein Triggers Plant Resistance to Insects and Pathogens as a Conserved HAMP.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Heat stress promotes osteogenic and odontogenic differentiation of stem cells from apical papilla via glucose-regulated protein 78-mediated autophagy.Journal of dental sciences · 2025Article
- Circ-0001283 Aggravates Cardiac Hypertrophy by Targeting Myosin Light Chain 3 Protein.Research (Washington, D.C.) · 2025Article
- The Role of theAnimals : an open access journal from MDPI · 2024Article
- Exploring the Regulation and Function ofGenes · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo determine the role of MYL4 regulation of lysosomal function and its disturbance in fibrotic atrial cardiomyopathy.
backgroundWe have previously demonstrated that the atrial-specific essential light chain protein MYL4 is required for atrial contractile, electrical, and structural integrity. MYL4 mutation/dysfunction leads to atrial fibrosis, standstill, and dysrhythmia. However, the underlying pathogenic mechanisms remain unclear. METHODS AND
resultsRats subjected to knock-in of a pathogenic MYL4 mutant (p.E11K) developed fibrotic atrial cardiomyopathy. Proteome analysis and single-cell RNA sequencing indicate enrichment of autophagy pathways in mutant-MYL4 atrial dysfunction. Immunofluorescence and electron microscopy revealed undegraded autophagic vesicles accumulated in MYL4
conclusionsMYL4 regulates autophagic flux in atrial cardiomyocytes via lysosomal mobility. MYL4 overexpression attenuates MYL4 p.E11K induced fibrotic atrial cardiomyopathy, while correcting autophagy and lysosomal function. These results provide a molecular basis for MYL4-mutant induced fibrotic atrial cardiomyopathy and identify a potential biological-therapy approach for the treatment of atrial fibrosis.
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