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The incidence of cardiovascular disease is predicted to further rise with the increase in obesity and diabetes and with the aging population. Even though the survival rate from ischaemic heart disease has improved over the past 30\u00a0years, many patients progress to a chronic pathological condition, known as cardiac hypertrophy that is associated with an increase in morbidity and mortality. Reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) and calcium play an essential role in mediating cardiac hypertrophy. The L\u2010type calcium channel is the main route for calcium influx into cardiac myocytes. There is now good evidence for a direct role for the L\u2010type calcium channel in the development of cardiac hypertrophy. Cysteines on the channel are targets for redox modification and glutathionylation of the channel can modulate the function of the channel protein leading to the onset of pathology. The cysteine responsible for modification of L\u2010type calcium channel function has now been identified. Detailed understanding of the role of cysteines as possible targets during oxidative stress may assist in designing therapy to prevent the development of hypertrophy and heart failure.<\/jats:p>","DOI":"10.1111\/1440-1681.12750","type":"journal-article","created":{"date-parts":[[2017,3,17]],"date-time":"2017-03-17T14:53:56Z","timestamp":1489762436000},"page":"46-54","source":"Crossref","is-referenced-by-count":29,"title":["The cardiac L\u2010type calcium channel alpha subunit is a target for direct redox modification during oxidative stress\u2014the role of cysteine residues in the alpha interacting domain"],"prefix":"10.1111","volume":"44","author":[{"given":"Padmapriya","family":"Muralidharan","sequence":"first","affiliation":[{"name":"School of Anatomy, Physiology and Human Biology University of Western Australia  Crawley WA Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0063-257X","authenticated-orcid":false,"given":"Henrietta","family":"Cserne Szappanos","sequence":"additional","affiliation":[{"name":"School of Anatomy, Physiology and Human Biology University of Western Australia  Crawley WA Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evan","family":"Ingley","sequence":"additional","affiliation":[{"name":"Harry Perkins Institute of Medical Research and Centre for Medical Research University of Western Australia  Perth WA Australia"},{"name":"School of Veterinary and Life Sciences Murdoch University  Murdoch WA Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Livia C","family":"Hool","sequence":"additional","affiliation":[{"name":"School of Anatomy, Physiology and Human Biology University of Western Australia  Crawley WA Australia"},{"name":"Victor Chang Cardiac Research Institute  Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,9,20]]},"reference":[{"key":"e_1_2_13_2_1","unstructured":"World Health Organisation.Non\u2010communicable diseases.Cardiovascular diseases (CVD).2014; Available at: URL:http:\/\/www.who.int\/mediacentre\/factsheets\/fs317\/en\/. 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