ArticleBMC medicine2020
The nSMase2/Smpd3 gene modulates the severity of muscular dystrophy and the emotional stress response in mdx mice.
Article in BMC medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Neurological impairments in Duchenne muscular dystrophy: A comprehensive review.Acta neurologica Belgica · 2026Review
- Key genes and processes affected by atorvastatin treatment in mouse diaphragm muscle.Archives of toxicology · 2025Article
- Resistance exercise training in older men reduces ATF4-activated and senescence-associated mRNAs in skeletal muscle.GeroScience · 2025Article
- Sphingomyelin phosphodiesterase 3 as a novel host factor inhibiting hepatitis B virus transcription.Virologica Sinica · 2025Article
- Application and perspective of CRISPR/Cas9 genome editing technology in human diseases modeling and gene therapy.Frontiers in genetics · 2024Review
- Partial restoration of brain dystrophin by tricyclo-DNA antisense oligonucleotides alleviates emotional deficits inMolecular therapy. Nucleic acids · 2023Article
- The unconditioned fear response in dystrophin-deficient mice is associated with adrenal and vascular function.Scientific reports · 2023Article
- Extracellular vesicles and Duchenne muscular dystrophy pathology: Modulators of disease progression.Frontiers in physiology · 2023Review
- Cardiovascular Disease in Duchenne Muscular Dystrophy: Overview and Insight Into Novel Therapeutic Targets.JACC. Basic to translational science · 2022Review
- Therapeutic Application of Extracellular Vesicles-Capsulated Adeno-Associated Virus Vector viaInternational journal of molecular sciences · 2022Review
- In sickness and in health: The functional role of extracellular vesicles in physiology and pathology in vivo: Part II: Pathology: Part II: Pathology.Journal of extracellular vesicles · 2022Review
- Nipping disease in the bud: nSMase2 inhibitors as therapeutics in extracellular vesicle-mediated diseases.Drug discovery today · 2021Review
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDuchenne muscular dystrophy (DMD) is a progressive, degenerative muscular disorder and cognitive dysfunction caused by mutations in the dystrophin gene. It is characterized by excess inflammatory responses in the muscle and repeated degeneration and regeneration cycles. Neutral sphingomyelinase 2/sphingomyelin phosphodiesterase 3 (nSMase2/Smpd3) hydrolyzes sphingomyelin in lipid rafts. This protein thus modulates inflammatory responses, cell survival or apoptosis pathways, and the secretion of extracellular vesicles in a Ca
methodsTo investigate the effects of the loss of nSMase2/Smpd3 on dystrophic muscles and its role in the abnormal behavior observed in DMD patients, we generated mdx mice lacking the nSMase2/Smpd3 gene (mdx:Smpd3 double knockout [DKO] mice).
resultsYoung mdx:Smpd3 DKO mice exhibited reduced muscular degeneration and decreased inflammation responses, but later on they showed exacerbated muscular necrosis. In addition, the abnormal stress response displayed by mdx mice was improved in the mdx:Smpd3 DKO mice, with the recovery of brain-derived neurotrophic factor (Bdnf) expression in the hippocampus.
conclusionsnSMase2/Smpd3-modulated lipid raft integrity is a potential therapeutic target for DMD.
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