P2X7 purinoceptor as a therapeutic target in muscular dystrophies
نویسندگان
چکیده
منابع مشابه
P2RX7 Purinoceptor: A Therapeutic Target for Ameliorating the Symptoms of Duchenne Muscular Dystrophy
BACKGROUND Duchenne muscular dystrophy (DMD) is the most common inherited muscle disease, leading to severe disability and death in young men. Death is caused by the progressive degeneration of striated muscles aggravated by sterile inflammation. The pleiotropic effects of the mutant gene also include cognitive and behavioral impairments and low bone density. Current interventions in DMD are pa...
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Muscular dystrophies are inherited myogenic disorders accompanied by progressive skeletal muscle weakness and degeneration. Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy and is caused by mutations in the gene that encodes the cytoskeletal protein dystrophin. The treatment for DMD is limited to glucocorticoids, which are associated with multiple side ...
متن کاملP2X7 purinoceptor alterations in dystrophic mdx mouse muscles: relationship to pathology and potential target for treatment
Duchenne muscular dystrophy (DMD) is a lethal inherited muscle disorder. Pathological characteristics of DMD skeletal muscles include, among others, abnormal Ca(2+) homeostasis and cell signalling. Here, in the mdx mouse model of DMD, we demonstrate significant P2X7 receptor abnormalities in isolated primary muscle cells and cell lines and in dystrophic muscles in vivo. P2X7 mRNA expression in...
متن کاملThe muscular dystrophies.
The muscular dystrophies are inherited myogenic disorders characterised by progressive muscle wasting and weakness of variable distribution and severity. They can be subdivided into several groups, including congenital forms, in accordance with the distribution of predominant muscle weakness: Duchenne and Becker; Emery-Dreifuss; distal; facioscapulohumeral; oculopharyngeal; and limb-girdle whic...
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ژورنال
عنوان ژورنال: Current Opinion in Pharmacology
سال: 2019
ISSN: 1471-4892
DOI: 10.1016/j.coph.2019.02.003