Original articleGene therapy prevents disruption of dystrophin-related proteins in a model of hereditary dilated cardiomyopathy in hamsters☆
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A novel scheme of dystrophin disruption for the progression of advanced heart failure
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2008, NeurotherapeuticsCitation Excerpt :The sarcoglycan null mice and the delta sarcoglycan-deficient cardiomyopathic hamsters (BIO14.6, BIO53.58, CHF147, TO-2) are also well-established animal models for sarcoglycan-deficient cardiomyopathy. The spectrum of therapeutic approaches that has been used to treat the dilated cardiomyopathy in the hamster models is very broad and reaches from classical pharmacotherapy approaches58,59 to gene replacement therapy,60–62 cellular therapies,63–65 and recombinant growth factor therapies.66–69 Despite numerous treatment studies in the cardiomyopathic hamster models over the past 40 years, many of which have been shown to be effective, no controlled trial to treat cardiomyopathy in patients with LGMD2C-F has been conducted so far.
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2017, Canadian Journal of Physiology and PharmacologyProspect of gene therapy for cardiomyopathy in hereditary muscular dystrophy
2016, Expert Opinion on Orphan DrugsSERCA2a gene therapy can improve symptomatic heart failure in δ-sarcoglycan-deficient animals
2014, Human Gene Therapy
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Presented at the International Society for Heart Research and International Union of Physiological Societies World Congress Satellite Meeting, Models of Cardiovascular Disease, 2–4 September 2001, Brisbane, Australia.