ArticleCell death & disease2019
sPIF promotes myoblast differentiation and utrophin expression while inhibiting fibrosis in Duchenne muscular dystrophy via the H19/miR-675/let-7 and miR-21 pathways.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Identification of potential microRNAs and KEGG pathways in denervation muscle atrophy based on meta-analysis.Scientific reports · 2021Pooled it
- CRISPR-Cas9-mediated upregulation of utrophin ameliorates Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- H19 lncRNA in programming prenatal development and DOHaD due to maternal obesity.Life sciences · 2026Review
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Identification of PANoptosis-Related Biomarkers in Hypertrophic Cardiomyopathy: Insights from Multi-Omics Analysis.Journal of inflammation research · 2026Article
- Temporal dynamics and functional implications of MiRNAs in denervation-induced skeletal muscle atrophy.Molecular biology reports · 2025Article
- Scientific and Technological Prospecting on Polymeric Particles Containing Extracellular Matrix Peptides for the Treatment of Duchenne Muscular Dystrophy.Recent advances in drug delivery and formulation · 2025Review
- Identification of reference microRNAs in skeletal muscle of a canine model of Duchenne muscular dystrophy.Wellcome open research · 2024Article
- The Long Noncoding RNA H19 Promotes Fibrotic Processes in Lens Epithelial Cells.Investigative ophthalmology & visual science · 2023Article
- Idiopathic inflammatory myopathy and non-coding RNA.Frontiers in immunology · 2023Review
- Promising therapeutic approaches of utrophin replacing dystrophin in the treatment of Duchenne muscular dystrophy.Fundamental research · 2022Review
- MicroRNAs in Dystrophinopathy.International journal of molecular sciences · 2022Review
- Regulation of Pyroptosis by ncRNA: A Novel Research Direction.Frontiers in cell and developmental biology · 2022Review
- Review
- Non-Coding RNAs as Regulators of Myogenesis and Postexercise Muscle Regeneration.International journal of molecular sciences · 2021Review
- Preimplantation factor modulates oligodendrocytes by H19-induced demethylation of NCOR2.JCI insight · 2021Article
- Utrophin modulator drugs as potential therapies for Duchenne and Becker muscular dystrophies.Neuropathology and applied neurobiology · 2021Article
- Article
- Neuron-Glia Crosstalk Plays a Major Role in the Neurotoxic Effects of KetamineFrontiers in cell and developmental biology · 2021Article
- PMO-based let-7c site blocking oligonucleotide (SBO) mediated utrophin upregulation in mdx mice, a therapeutic approach for Duchenne muscular dystrophy (DMD).Scientific reports · 2020Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a progressive, lethal, X-linked disease of skeletal and cardiac muscles caused by mutations in the dystrophin gene. Loss of dystrophin leads to muscle fiber damage and impairment of satellite cell asymmetric division, which are essential for muscle regeneration. These processes ultimately result in muscle wasting and the replacement of the degenerating muscles by fibrogenic cells, a process that leads to the generation of fibrotic tissues. Preimplantation factor (PIF) is an evolutionary conserved 15-amino acid peptide secreted by viable mammalian embryos. Synthetic PIF (sPIF) reproduces the protective/regenerative effects of the endogenous peptide in immune disorders and transplantation models. In this study, we demonstrated that sPIF treatment promoted mouse and human myoblast differentiation and inhibited the expression of collagen 1A1, collagen 1A2, and TGF-β in DMD patient-derived myoblasts. Additionally, sPIF increased the expression of utrophin, a homolog of dystrophin protein. sPIF effects were mediated via the upregulation of lncRNA H19 and miR-675 and downregulation of let-7. sPIF also inhibited the expression of miR-21, a major fibrosis regulator. The administration of sPIF in mdx mice significantly decreased serum creatine kinase and collagen I and collagen IV expression in the diaphragm, whereas it increased utrophin expression in the diaphragm, heart and quadriceps muscles. In conclusion, sPIF promoted the differentiation of DMD myoblasts, increased utrophin expression via the H19/miRNA-675/let-7 pathway, and reduced muscle fibrosis possibly via the upregulation of miR-675 and inhibition of miR-21 expression. These findings strongly support pursuing sPIF as a potential therapeutic agent for DMD. Moreover, the completion of an sPIF phase I safety trial will further promote the use of sPIF for the treatment of muscular dystrophies.
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