ArticleJournal of cachexia, sarcopenia and muscle2018
Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.
Article in Journal of cachexia, sarcopenia and muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Obestatin: canonical and unexpected functions.Reviews in endocrine & metabolic disorders · 2026Review
- Obestatin Treatment Counteracts Muscle Wasting by Reactivation of Autophagy in Duchenne Muscular Dystrophy.MedComm · 2026Article
- Obestatin treatment links mitochondrial homeostasis and skeletal muscle repair in Duchenne muscle dystrophy.Molecular biomedicine · 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
- A Brief Review of Duchenne Muscular Dystrophy Treatment Options, with an Emphasis on Two Novel Strategies.Biomedicines · 2023Review
- Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation.Nature communications · 2022Article
- Utrophin modulator drugs as potential therapies for Duchenne and Becker muscular dystrophies.Neuropathology and applied neurobiology · 2021Article
- Obestatin signalling counteracts glucocorticoid-induced skeletal muscle atrophy via NEDD4/KLF15 axis.Journal of cachexia, sarcopenia and muscle · 2021Article
- Ixazomib, an oral proteasome inhibitor, exhibits potential effect in dystrophin-deficient mdx mice.International journal of experimental pathology · 2021Article
- Using a State-of-the-Art Toolbox to Evaluate Molecular and Functional Readouts of Antisense Oligonucleotide-Induced Exon Skipping inNucleic acid therapeutics · 2020Article
- The Journal of Cachexia, Sarcopenia and Muscle stays the front-runner in geriatrics and gerontology.Journal of cachexia, sarcopenia and muscle · 2019Article
- Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.Journal of cachexia, sarcopenia and muscle · 2018Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study was performed to test the therapeutic potential of obestatin, an autocrine anabolic factor regulating skeletal muscle repair, to ameliorate the Duchenne muscular dystrophy (DMD) phenotype. METHODS AND
resultsUsing a multidisciplinary approach, we characterized the ageing-related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4-, 8-, and 18-week-old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8-week-old mdx mice (n = 5/group). The findings were extended to in vitro effects on human immortalized DMD myotubes. An analysis of TAs revealed an age-related loss of preproghrelin expression, as precursor of obestatin, in mdx mice. Administration of obestatin resulted in a significant increase in tetanic specific force (33.0% ± 1.5%, P < 0.05), compared with control mdx mice. Obestatin-treated TAs were characterized by reduction of fibres with centrally located nuclei (10.0% ± 1.2%, P < 0.05) together with an increase in the number of type I fibres (25.2% ± 1.7%, P < 0.05) associated to histone deacetylases/myocyte enhancer factor-2 and peroxisome proliferator-activated receptor-gamma coactivator 1α axis, and down-regulation of ubiquitin E3-ligases by inactivation of FoxO1/4, indexes of muscle atrophy. Obestatin reduced the level of contractile damage and tissue fibrosis. These observations correlated with decline in serum creatine kinase (58.8 ± 15.2, P < 0.05). Obestatin led to stabilization of the sarcolemma by up-regulation of utrophin, α-syntrophin, β-dystroglycan, and α7β1-integrin proteins. These pathways were also operative in human DMD myotubes.
conclusionsThese results highlight the potential of obestatin as a peptide therapeutic for preserving muscle integrity in DMD, thus allowing a better efficiency of gene or cell therapy in a combined therapeutic approach.
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