{"PubmedArticle":{"MedlineCitation":{"@attributes":{"Status":"MEDLINE","Owner":"NLM","IndexingMethod":"Manual"},"PMID":{"@attributes":{"Version":"1"},"@text":"26676145"},"DateCompleted":{"Year":"2016","Month":"02","Day":"16"},"DateRevised":{"Year":"2022","Month":"03","Day":"21"},"Article":{"@attributes":{"PubModel":"Print"},"Journal":{"ISSN":{"@attributes":{"IssnType":"Electronic"},"@text":"1522-1210"},"JournalIssue":{"@attributes":{"CitedMedium":"Internet"},"Volume":"96","Issue":"1","PubDate":{"Year":"2016","Month":"Jan"}},"Title":"Physiological reviews","ISOAbbreviation":"Physiol Rev"},"ArticleTitle":"Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.","Pagination":{"StartPage":"253","EndPage":"305","MedlinePgn":"253-305"},"ELocationID":[{"@attributes":{"EIdType":"doi","ValidYN":"Y"},"@text":"10.1152\/physrev.00007.2015"}],"Abstract":{"AbstractText":["Dystrophin is a long rod-shaped protein that connects the subsarcolemmal cytoskeleton to a complex of proteins in the surface membrane (dystrophin protein complex, DPC), with further connections via laminin to other extracellular matrix proteins. Initially considered a structural complex that protected the sarcolemma from mechanical damage, the DPC is now known to serve as a scaffold for numerous signaling proteins. Absence or reduced expression of dystrophin or many of the DPC components cause the muscular dystrophies, a group of inherited diseases in which repeated bouts of muscle damage lead to atrophy and fibrosis, and eventually muscle degeneration. The normal function of dystrophin is poorly defined. In its absence a complex series of changes occur with multiple muscle proteins showing reduced or increased expression or being modified in various ways. In this review, we will consider the various proteins whose expression and function is changed in muscular dystrophies, focusing on Ca(2+)-permeable channels, nitric oxide synthase, NADPH oxidase, and caveolins. Excessive Ca(2+) entry, increased membrane permeability, disordered caveolar function, and increased levels of reactive oxygen species are early changes in the disease, and the hypotheses for these phenomena will be critically considered. The aim of the review is to define the early damage pathways in muscular dystrophy which might be appropriate targets for therapy designed to minimize the muscle degeneration and slow the progression of the disease."],"CopyrightInformation":"Copyright \u00a9 2016 the American Physiological Society."},"AuthorList":{"@attributes":{"CompleteYN":"Y"},"Author":[{"@attributes":{"ValidYN":"Y"},"LastName":"Allen","ForeName":"David G","Initials":"DG","AffiliationInfo":[{"Affiliation":"Sydney Medical School &amp; Bosch Institute, University of Sydney, New South Wales, Australia; and Department of Physiology &amp; Biophysics, University of Washington, Seattle, Washington."}]},{"@attributes":{"ValidYN":"Y"},"LastName":"Whitehead","ForeName":"Nicholas P","Initials":"NP","AffiliationInfo":[{"Affiliation":"Sydney Medical School &amp; Bosch Institute, University of Sydney, New South Wales, Australia; and Department of Physiology &amp; Biophysics, University of Washington, Seattle, Washington."}]},{"@attributes":{"ValidYN":"Y"},"LastName":"Froehner","ForeName":"Stanley C","Initials":"SC","AffiliationInfo":[{"Affiliation":"Sydney Medical School &amp; Bosch Institute, University of Sydney, New South Wales, Australia; and Department of Physiology &amp; Biophysics, University of Washington, Seattle, Washington."}]}]},"Language":["eng"],"GrantList":{"@attributes":{"CompleteYN":"Y"},"Grant":[{"GrantID":"R01 NS33145","Acronym":"NS","Agency":"NINDS NIH HHS","Country":"United States"},{"GrantID":"P01 NS04678","Acronym":"NS","Agency":"NINDS NIH HHS","Country":"United States"},{"GrantID":"R01 NS033145","Acronym":"NS","Agency":"NINDS NIH HHS","Country":"United States"},{"GrantID":"R21 NS088691","Acronym":"NS","Agency":"NINDS NIH HHS","Country":"United States"},{"GrantID":"R01AR056221","Acronym":"AR","Agency":"NIAMS NIH HHS","Country":"United States"}]},"PublicationTypeList":{"PublicationType":[{"@attributes":{"UI":"D016428"},"@text":"Journal Article"},{"@attributes":{"UI":"D052061"},"@text":"Research Support, N.I.H., Extramural"},{"@attributes":{"UI":"D016454"},"@text":"Review"}]}},"MedlineJournalInfo":{"Country":"United States","MedlineTA":"Physiol Rev","NlmUniqueID":"0231714","ISSNLinking":"0031-9333"},"ChemicalList":{"Chemical":[{"RegistryNumber":"0","NameOfSubstance":{"@attributes":{"UI":"D016189"},"@text":"Dystrophin"}},{"RegistryNumber":"0","NameOfSubstance":{"@attributes":{"UI":"D017382"},"@text":"Reactive Oxygen Species"}},{"RegistryNumber":"31C4KY9ESH","NameOfSubstance":{"@attributes":{"UI":"D009569"},"@text":"Nitric Oxide"}},{"RegistryNumber":"SY7Q814VUP","NameOfSubstance":{"@attributes":{"UI":"D002118"},"@text":"Calcium"}}]},"CitationSubset":["IM"],"MeshHeadingList":{"MeshHeading":[{"DescriptorName":{"@attributes":{"UI":"D000818","MajorTopicYN":"N"},"@text":"Animals"}},{"DescriptorName":{"@attributes":{"UI":"D002118","MajorTopicYN":"N"},"@text":"Calcium"},"QualifierName":[{"@attributes":{"UI":"Q000378","MajorTopicYN":"Y"},"@text":"metabolism"}]},{"DescriptorName":{"@attributes":{"UI":"D020013","MajorTopicYN":"N"},"@text":"Calcium Signaling"}},{"DescriptorName":{"@attributes":{"UI":"D016189","MajorTopicYN":"N"},"@text":"Dystrophin"},"QualifierName":[{"@attributes":{"UI":"Q000172","MajorTopicYN":"N"},"@text":"deficiency"},{"@attributes":{"UI":"Q000235","MajorTopicYN":"N"},"@text":"genetics"},{"@attributes":{"UI":"Q000378","MajorTopicYN":"Y"},"@text":"metabolism"}]},{"DescriptorName":{"@attributes":{"UI":"D005786","MajorTopicYN":"N"},"@text":"Gene Expression Regulation"}},{"DescriptorName":{"@attributes":{"UI":"D006801","MajorTopicYN":"N"},"@text":"Humans"}},{"DescriptorName":{"@attributes":{"UI":"D024510","MajorTopicYN":"N"},"@text":"Muscle Development"}},{"DescriptorName":{"@attributes":{"UI":"D018482","MajorTopicYN":"N"},"@text":"Muscle, Skeletal"},"QualifierName":[{"@attributes":{"UI":"Q000378","MajorTopicYN":"Y"},"@text":"metabolism"},{"@attributes":{"UI":"Q000473","MajorTopicYN":"N"},"@text":"pathology"},{"@attributes":{"UI":"Q000503","MajorTopicYN":"N"},"@text":"physiopathology"}]},{"DescriptorName":{"@attributes":{"UI":"D009136","MajorTopicYN":"N"},"@text":"Muscular Dystrophies"},"QualifierName":[{"@attributes":{"UI":"Q000235","MajorTopicYN":"N"},"@text":"genetics"},{"@attributes":{"UI":"Q000378","MajorTopicYN":"Y"},"@text":"metabolism"},{"@attributes":{"UI":"Q000473","MajorTopicYN":"N"},"@text":"pathology"},{"@attributes":{"UI":"Q000503","MajorTopicYN":"N"},"@text":"physiopathology"}]},{"DescriptorName":{"@attributes":{"UI":"D009569","MajorTopicYN":"N"},"@text":"Nitric Oxide"},"QualifierName":[{"@attributes":{"UI":"Q000378","MajorTopicYN":"Y"},"@text":"metabolism"}]},{"DescriptorName":{"@attributes":{"UI":"D017382","MajorTopicYN":"N"},"@text":"Reactive Oxygen Species"},"QualifierName":[{"@attributes":{"UI":"Q000378","MajorTopicYN":"Y"},"@text":"metabolism"}]},{"DescriptorName":{"@attributes":{"UI":"D012038","MajorTopicYN":"N"},"@text":"Regeneration"}},{"DescriptorName":{"@attributes":{"UI":"D015398","MajorTopicYN":"Y"},"@text":"Signal Transduction"}}]}},"PubmedData":{"History":{"PubMedPubDate":[{"@attributes":{"PubStatus":"entrez"},"Year":"2015","Month":"12","Day":"18","Hour":"6","Minute":"0"},{"@attributes":{"PubStatus":"pubmed"},"Year":"2015","Month":"12","Day":"18","Hour":"6","Minute":"0"},{"@attributes":{"PubStatus":"medline"},"Year":"2016","Month":"2","Day":"18","Hour":"6","Minute":"0"},{"@attributes":{"PubStatus":"pmc-release"},"Year":"2017","Month":"1","Day":"1"}]},"PublicationStatus":"ppublish","ArticleIdList":{"ArticleId":[{"@attributes":{"IdType":"pubmed"},"@text":"26676145"},{"@attributes":{"IdType":"pmc"},"@text":"PMC4698395"},{"@attributes":{"IdType":"doi"},"@text":"10.1152\/physrev.00007.2015"},{"@attributes":{"IdType":"pii"},"@text":"96\/1\/253"}]},"ReferenceList":[{"Reference":[{"Citation":"Aartsma-Rus A, Muntoni F. 194th ENMC International Workshop. 3rd ENMC workshop on exon skipping: towards clinical application of antisense-mediated exon skipping for Duchenne muscular dystrophy 8\u201310 December 2012, Naarden, The Netherlands. 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