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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2017,12,12]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    The pathological Duchenne muscular dystrophy (DMD) muscles show increased stretch-induced intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and nitrosative stress. Whether there is a link between the two, and how the former impacts the nitrosylated proteome, is unknown. Here, we report that transient receptor potential channel 6 (Trpc6) modulates increased nitrosative stress in dmd\n                    <jats:sup>mdx<\/jats:sup>\n                    :utrn\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice, as reflected by an increase in protein S-nitrosylation, and provide a broad high-throughput analysis of S-nitrosylation in this model. We found that S-nitrosothiol targets are conserved in dmd\n                    <jats:sup>mdx<\/jats:sup>\n                    :utrn\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    myocardium, but intensified in a Trpc6-dependent manner. Restoration of more normal S-nitrosylation profiles in dmd\n                    <jats:sup>mdx<\/jats:sup>\n                    :utrn\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mouse hearts lacking Trpc6 corresponds to improved cardiac function and reduced fibrosis. These findings link Trpc6-mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling and nitrosative stress in the redox pathobiology of DMD.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1712623114","type":"journal-article","created":{"date-parts":[[2017,12,12]],"date-time":"2017-12-12T15:25:59Z","timestamp":1513092359000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":33,"title":["Transient receptor potential channel 6 regulates abnormal cardiac S-nitrosylation in Duchenne muscular dystrophy"],"prefix":"10.1073","volume":"114","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1165-8388","authenticated-orcid":false,"given":"Heaseung Sophia","family":"Chung","sequence":"first","affiliation":[{"name":"Advanced Clinical BioSystems Research Institute, Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grace E.","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald J.","family":"Holewinski","sequence":"additional","affiliation":[{"name":"Advanced Clinical BioSystems Research Institute, Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vidya","family":"Venkatraman","sequence":"additional","affiliation":[{"name":"Advanced Clinical BioSystems Research Institute, Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guangshuo","family":"Zhu","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Djahida","family":"Bedja","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Kass","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205;"},{"name":"Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer E.","family":"Van Eyk","sequence":"additional","affiliation":[{"name":"Advanced Clinical BioSystems Research Institute, Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048;"},{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2017,11,29]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"crossref","first-page":"762","DOI":"10.1038\/nrm2024","article-title":"Molecular mechanisms of muscular dystrophies: Old and new players","volume":"7","author":"Davies KE","year":"2006","unstructured":"KE Davies, KJ Nowak, Molecular mechanisms of muscular dystrophies: Old and new players. 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