{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T15:06:53Z","timestamp":1791558413906,"version":"4.3.4"},"reference-count":67,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2019,12,5]],"date-time":"2019-12-05T00:00:00Z","timestamp":1575504000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JCM"],"abstract":"<jats:p>Duchenne and Becker muscular dystrophies (DMD\/BMD) result in progressive weakness of skeletal and cardiac muscles due to the deficiency of functional dystrophin. Respiratory failure is a leading cause of mortality in DMD patients; however, improved management of the respiratory symptoms have increased patients\u2019 life expectancy, thereby also increasing the clinical relevance of heart disease. In fact, the prevalence of cardiomyopathy, which significantly contributes to mortality in DMD patients, increases with age and disease progression, so that over 95% of adult patients has cardiomyopathy signs. We here review the current literature featuring the metabolic alterations observed in the dystrophic heart of the mdx mouse, i.e., the best-studied animal model of the disease, and discuss their pathophysiological role in the DMD heart. It is well assessed that dystrophin deficiency is associated with pathological alterations of lipid metabolism, intracellular calcium levels, neuronal nitric oxide (NO) synthase localization, and NO and reactive oxygen species production. These metabolic stressors contribute to impair the function of the cardiac mitochondrial bulk, which has a relevant pathophysiological role in the development of cardiomyopathy. In fact, mitochondrial dysfunction becomes more severe as the dystrophic process progresses, thereby indicating it may be both the cause and the consequence of the dystrophic process in the DMD heart.<\/jats:p>","DOI":"10.3390\/jcm8122151","type":"journal-article","created":{"date-parts":[[2019,12,5]],"date-time":"2019-12-05T11:16:31Z","timestamp":1575544591000},"page":"2151","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Metabolic Alterations in Cardiomyocytes of Patients with Duchenne and Becker Muscular Dystrophies"],"prefix":"10.3390","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4255-7312","authenticated-orcid":false,"given":"Gabriella","family":"Esposito","sequence":"first","affiliation":[{"name":"Department of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, Via Pansini 5, 80131 Naples, Italy"},{"name":"CEINGE Advanced Biotechnologies, Via Gaetano Salvatore 486, 80145 Naples, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6815-7093","authenticated-orcid":false,"given":"Antonella","family":"Carsana","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, Via Pansini 5, 80131 Naples, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2019,12,5]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"809","DOI":"10.1083\/jcb.122.4.809","article-title":"A role for the dystrophin-glycoprotein complex as a transmembrane linker between laminin and actin","volume":"122","author":"Ervasti","year":"1993","journal-title":"J. Cell. Biol."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"3710","DOI":"10.1073\/pnas.90.8.3710","article-title":"Dystrophin protects the sarcolemma from stresses developed during muscle contraction","volume":"90","author":"Petrof","year":"1993","journal-title":"Proc. Natl. Acad. Sci. USA"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"1575","DOI":"10.1002\/mus.1192","article-title":"The dystrophin-glycoprotein complex, cellular signaling, and the regulation of cell survival in the muscular dystrophies","volume":"24","author":"Rando","year":"2001","journal-title":"Muscle Nerve"},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"484","DOI":"10.1038\/sj.embor.7400140","article-title":"Dystroglycan, a scaffold for the ERK\u2013MAP kinase cascade","volume":"5","author":"Spence","year":"2004","journal-title":"EMBO Rep."},{"key":"ref_5","doi-asserted-by":"crossref","first-page":"397","DOI":"10.1046\/j.1365-201X.1996.201000.x","article-title":"Membrane abnormalities and Ca homeostasis in muscles of the mdx mouse, an animal model of the Duchenne muscular dystrophy: A review","volume":"156","author":"Gillis","year":"1996","journal-title":"Acta Physiol. Scand."},{"key":"ref_6","unstructured":"Scriver, C.R., Beaudet, A.L., Valle, D., and Sly, W.S. (2001). The muscular dystrophies. The Metabolic and Molecular Bases of Inherited Disease, McGraw Hill. [8th ed.]."},{"key":"ref_7","doi-asserted-by":"crossref","first-page":"671","DOI":"10.1007\/s10072-019-03764-z","article-title":"Genetic neuromuscular disorders: Living the era of a therapeutic revolution. Part 2: Diseases of motor neuron and skeletal muscle","volume":"40","author":"Vita","year":"2019","journal-title":"Neurol. Sci."},{"key":"ref_8","doi-asserted-by":"crossref","first-page":"2239","DOI":"10.1515\/cclm-2013-0209","article-title":"Prenatal molecular diagnoses of inherited neuromuscular diseases: Duchenne\/Becker muscular dystrophy, myotonic dystrophy type 1 and spinal muscular atrophy","volume":"51","author":"Esposito","year":"2013","journal-title":"Clin. Chem. Lab. Med."},{"key":"ref_9","doi-asserted-by":"crossref","first-page":"1057","DOI":"10.1038\/jhg.2017.84","article-title":"Precise mapping of 17 deletion breakpoints within the central hotspot deletion region (introns 50 and 51) of the DMD gene","volume":"62","author":"Esposito","year":"2017","journal-title":"J. Hum. Genet."},{"key":"ref_10","doi-asserted-by":"crossref","first-page":"64","DOI":"10.2353\/jmoldx.2007.060056","article-title":"A larger spectrum of intragenic STRs improves linkage analysis and localization of intragenic recombination detection in the dystrophin gene: An analysis of 93 families from Southern Italy","volume":"9","author":"Carsana","year":"2007","journal-title":"J. Mol. Diagn."},{"key":"ref_11","doi-asserted-by":"crossref","first-page":"99","DOI":"10.1586\/14779072.5.1.99","article-title":"Cardiomyopathy of Duchenne muscular dystrophy: Pathogenesis and prospect of membrane sealants as a new therapeutic approach","volume":"5","author":"Townsend","year":"2007","journal-title":"Expert. Rev. Cardiovasc. Ther."},{"key":"ref_12","doi-asserted-by":"crossref","first-page":"618","DOI":"10.1016\/0002-8703(94)90672-6","article-title":"Prevalence of left ventricular systolic dysfunction in Duchenne muscular dystrophy: An echocardiographic study","volume":"127","author":"Tertrain","year":"1994","journal-title":"Am. Heart J."},{"key":"ref_13","doi-asserted-by":"crossref","first-page":"1655","DOI":"10.1096\/fj.01-0030fje","article-title":"Dystrophin-deficient cardiomyocytes are abnormally vulnerable to mechanical stress-induced contractile failure and injury","volume":"15","author":"Danialou","year":"2001","journal-title":"Faseb J."},{"key":"ref_14","doi-asserted-by":"crossref","first-page":"67","DOI":"10.1161\/CIRCIMAGING.110.960740","article-title":"Cardiac involvement in patients with muscular dystrophies: Magnetic resonance imaging phenotype and genotypic considerations","volume":"4","author":"Verhaert","year":"2011","journal-title":"Circ. Cardiovasc. Imaging"},{"key":"ref_15","first-page":"2547","article-title":"A 15-year molecular analysis of Duchenne\/Becker muscular dystrophy: Genetic features in a large cohort","volume":"2E","author":"Carsana","year":"2010","journal-title":"Front. Biosci."},{"key":"ref_16","doi-asserted-by":"crossref","first-page":"130","DOI":"10.1093\/hmg\/ddv460","article-title":"Effect of genetic background on the dystrophic phenotype in mdx mice","volume":"25","author":"Coley","year":"2016","journal-title":"Hum. Mol. Genet."},{"key":"ref_17","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1155\/2015\/131436","article-title":"Biochemical and Functional Comparisons of mdx and Sgcg(-\/-) Muscular Dystrophy Mouse Models","volume":"2015","author":"Roberts","year":"2015","journal-title":"BioMed Res. Int."},{"key":"ref_18","doi-asserted-by":"crossref","first-page":"1021","DOI":"10.1016\/j.mehy.2015.08.015","article-title":"Revisiting the dystrophin-ATP connection: How half a century of research still implicates mitochondrial dysfunction in Duchenne Muscular Dystrophy aetiology","volume":"85","author":"Timpani","year":"2015","journal-title":"Med. Hypotheses"},{"key":"ref_19","doi-asserted-by":"crossref","first-page":"777","DOI":"10.7326\/M14-2385","article-title":"The PRISMA extension statement for reporting of systematic reviews incorporating network meta-analyses of health care interventions: Checklist and explanations","volume":"162","author":"Hutton","year":"2015","journal-title":"Ann. Intern. Med."},{"key":"ref_20","doi-asserted-by":"crossref","first-page":"163","DOI":"10.1016\/j.mri.2017.01.001","article-title":"Abnormal lipid metabolism in skeletal muscle tissue of patients with muscular dystrophy: In vitro, high-resolution NMR spectroscopy based observation in early phase of the disease","volume":"38","author":"Srivastava","year":"2017","journal-title":"Magn. Reson. Imaging"},{"key":"ref_21","doi-asserted-by":"crossref","first-page":"19","DOI":"10.1186\/s13395-017-0135-9","article-title":"Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy","volume":"7","author":"Milad","year":"2017","journal-title":"Skelet. Muscle"},{"key":"ref_22","doi-asserted-by":"crossref","first-page":"705","DOI":"10.1080\/15548627.2016.1144005","article-title":"Enhanced autophagy as a potential mechanism for the improved physiological function by simvastatin in muscular dystrophy","volume":"12","author":"Whitehead","year":"2016","journal-title":"Autophagy"},{"key":"ref_23","doi-asserted-by":"crossref","first-page":"1507","DOI":"10.1007\/s00018-019-03006-7","article-title":"Targeting angiogenesis in Duchenne muscular dystrophy","volume":"76","author":"Podkalicka","year":"2019","journal-title":"Cell Mol. Life Sci."},{"key":"ref_24","doi-asserted-by":"crossref","first-page":"396","DOI":"10.1016\/j.nmd.2011.02.016","article-title":"Idebenone as a novel, therapeutic approach for Duchenne muscular dystrophy: Results from a 12 month, double-blind, randomized placebo-controlled trial","volume":"21","author":"Buyse","year":"2011","journal-title":"Neuromuscul. Disord."},{"key":"ref_25","doi-asserted-by":"crossref","first-page":"1748","DOI":"10.1016\/S0140-6736(15)60025-3","article-title":"Efficacy of idebenone on respiratory function in patients with Duchenne muscular dystrophy not using glucocorticoids (DELOS): A double-blind randomized placebo-controlled phase 3 trial","volume":"385","author":"Buyse","year":"2015","journal-title":"Lancet"},{"key":"ref_26","doi-asserted-by":"crossref","first-page":"508","DOI":"10.1002\/ppul.23547","article-title":"Treatment effect of idebenone on inspiratory function in patients with Duchenne muscular dystrophy","volume":"52","author":"Buyse","year":"2017","journal-title":"Pediatr. Pulmonol."},{"key":"ref_27","doi-asserted-by":"crossref","first-page":"100","DOI":"10.1186\/s13023-017-0652-y","article-title":"Therapeutic strategies to address neuronal nitric oxide synthase deficiency and the loss of nitric oxide bioavailability in Duchenne Muscular Dystrophy","volume":"12","author":"Timpani","year":"2017","journal-title":"Orphanet J. Rare Dis."},{"key":"ref_28","doi-asserted-by":"crossref","first-page":"14","DOI":"10.1111\/j.1749-6632.1966.tb41151.x","article-title":"Hereditary myopathy in the Syrian hamster: Studies on pathogenesis","volume":"138","author":"Homburger","year":"1966","journal-title":"Ann. N. Y. Acad. Sci."},{"key":"ref_29","doi-asserted-by":"crossref","first-page":"69","DOI":"10.1159\/000393365","article-title":"Disease models in Syrian hamsters","volume":"16","author":"Homburger","year":"1972","journal-title":"Prog. Exp. Tumor Res."},{"key":"ref_30","first-page":"443","article-title":"Changes in electrolyte and lipid contents of the myopathic hamster (UM-X7.1) skeletal and cardiac muscles","volume":"7","author":"Borowski","year":"1974","journal-title":"Res. Commun. Chem. Pathol. Pharmacol."},{"key":"ref_31","doi-asserted-by":"crossref","first-page":"229","DOI":"10.1016\/0022-2828(72)90060-0","article-title":"Phospholipid and cholesterol content of ventricular tissue from the cardiomyopathic Syrian hamster","volume":"4","author":"Owens","year":"1972","journal-title":"J. Mol. Cell. Cardiol."},{"key":"ref_32","doi-asserted-by":"crossref","first-page":"96","DOI":"10.1016\/S0022-2275(20)32340-3","article-title":"Insulin deficiency and reduced expression of lipogenic enzymes in cardiomyopathic hamster","volume":"42","author":"Vecchini","year":"2001","journal-title":"J. Lipid Res."},{"key":"ref_33","doi-asserted-by":"crossref","first-page":"13","DOI":"10.1002\/nbm.1419","article-title":"High resolution NMR based analysis of serum lipids in Duchenne muscular dystrophy patients and its possible diagnostic significance","volume":"23","author":"Srivastava","year":"2010","journal-title":"NMR Biomed."},{"key":"ref_34","doi-asserted-by":"crossref","unstructured":"Barbieri, E., and Sestili, P. (2012). Reactive oxygen species in skeletal muscle signaling. J. Signal. Transduct., 982794.","DOI":"10.1155\/2012\/982794"},{"key":"ref_35","doi-asserted-by":"crossref","first-page":"3716","DOI":"10.1172\/JCI120849","article-title":"Mitochondrial dysfunction in pathophysiology of heart failure","volume":"128","author":"Zhou","year":"2018","journal-title":"J. Clin. Investig."},{"key":"ref_36","doi-asserted-by":"crossref","first-page":"253","DOI":"10.1152\/physrev.00007.2015","article-title":"Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy","volume":"96","author":"Allen","year":"2016","journal-title":"Physiol. Rev."},{"key":"ref_37","doi-asserted-by":"crossref","first-page":"310","DOI":"10.1016\/j.yjmcc.2009.09.004","article-title":"Alterations in mitochondrial function as a harbinger of cardiomyopathy: Lessons from the dystrophic heart","volume":"48","author":"Burelle","year":"2010","journal-title":"J. Mol. Cell. Cardiol."},{"key":"ref_38","first-page":"3403075","article-title":"The Mitochondrial Permeability Transition in Mitochondrial Disorders","volume":"2019","author":"Forte","year":"2019","journal-title":"Oxid. Med. Cell. Longev."},{"key":"ref_39","doi-asserted-by":"crossref","unstructured":"Laher, I. (2014). Reactive Oxygen Species and Muscular Dystrophy. Systems Biology of Free Radicals and Antioxidants, Springer.","DOI":"10.1007\/978-3-642-30018-9"},{"key":"ref_40","doi-asserted-by":"crossref","first-page":"2609847","DOI":"10.1155\/2018\/2609847","article-title":"Formyl peptide receptor 1 modulates endothelial cell functions by NADPH oxidase-dependent VEGFR2 transactivation","volume":"2018","author":"Cattaneo","year":"2018","journal-title":"Oxid. Med. Cell Longev."},{"key":"ref_41","doi-asserted-by":"crossref","first-page":"H144","DOI":"10.1152\/ajpheart.00522.2010","article-title":"Stress-induced opening of the permeability transition pore in the dystrophin-deficient heart is attenuated by acute treatment with sildenafil","volume":"300","author":"Ascah","year":"2010","journal-title":"Am. J. Physiol. Heart. Circ. Physiol."},{"key":"ref_42","doi-asserted-by":"crossref","unstructured":"Hughes, M.C., Ramos, S.V., Turnbull, P.C., Edgett, B.A., Huber, J.S., Polidovitch, N., Schlattner, U., Backx, P.H., Simpson, J.A., and Perry, C.G.R. (2019). Impairments in left ventricular mitochondrial bioenergetics precede overt cardiac dysfunction and remodelling in Duchenne muscular dystrophy. J. Physiol.","DOI":"10.1113\/JP277306"},{"key":"ref_43","doi-asserted-by":"crossref","first-page":"H710","DOI":"10.1152\/ajpheart.00890.2013","article-title":"NADPH oxidase-2 inhibition restores contractility and intracellular calcium handling and reduces arrhythmogenicity in dystrophic cardiomyopathy","volume":"307","author":"Gonzalez","year":"2014","journal-title":"Am. J. Physiol. Heart Circ. Physiol."},{"key":"ref_44","doi-asserted-by":"crossref","first-page":"H1969","DOI":"10.1152\/ajpheart.00489.2007","article-title":"The Role of Reactive Oxygen Species in the Hearts of Dystrophin-Deficient Mdx Mice","volume":"293","author":"Williams","year":"2007","journal-title":"Am. J. Physiol. Circ. Physiol."},{"key":"ref_45","doi-asserted-by":"crossref","first-page":"743","DOI":"10.1016\/0092-8674(95)90471-9","article-title":"Nitric oxide synthase complexed with dystrophin and absent from skeletal muscle sarcolemma in Duchenne muscular dystrophy","volume":"82","author":"Brenman","year":"1995","journal-title":"Cell"},{"key":"ref_46","doi-asserted-by":"crossref","first-page":"57","DOI":"10.1016\/j.pharmthera.2004.11.003","article-title":"Cardiac nitric oxide: Emerging role for nNOS in regulating physiological function","volume":"106","author":"Danson","year":"2005","journal-title":"Pharmacol. Ther."},{"key":"ref_47","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1042\/BJ20120787","article-title":"Nitric Oxide Signalling Pathway in Duchenne Muscular Dystrophy Mice: Up-Regulation of L-Arginine Transporters","volume":"449","author":"Ramachandran","year":"2013","journal-title":"Biochem. J."},{"key":"ref_48","doi-asserted-by":"crossref","first-page":"964","DOI":"10.1016\/j.nmd.2015.09.011","article-title":"Neuronal nitric oxide synthase localizes to utrophin expressing intercalated discs and stabilizes their structural integrity","volume":"25","author":"Gonzalez","year":"2015","journal-title":"Neuromuscul. Disord."},{"key":"ref_49","doi-asserted-by":"crossref","first-page":"1921","DOI":"10.1093\/hmg\/ddi197","article-title":"Cardiomyopathy in dystrophin-deficient hearts is prevented by expression of a neuronal nitric oxide synthase transgene in the myocardium","volume":"14","author":"Jordan","year":"2005","journal-title":"Hum. Mol. Genet."},{"key":"ref_50","doi-asserted-by":"crossref","first-page":"13165","DOI":"10.1073\/pnas.1004509107","article-title":"Genetic inhibition of PKA phosphorylation of RyR2 prevents dystrophic cardiomyopathy","volume":"107","author":"Sarma","year":"2010","journal-title":"Proc. Natl. Acad. Sci. USA"},{"key":"ref_51","doi-asserted-by":"crossref","first-page":"592","DOI":"10.1016\/j.hrthm.2012.12.016","article-title":"Inhibition of CaMKII phosphorylation of RyR2 prevents inducible ventricular arrhythmias in mice with Duchenne muscular dystrophy","volume":"10","author":"Ather","year":"2013","journal-title":"Heart Rhythm"},{"key":"ref_52","doi-asserted-by":"crossref","first-page":"1559","DOI":"10.1073\/pnas.0908540107","article-title":"Leaky RyR2 trigger ventricular arrhythmias in Duchenne muscular dystrophy","volume":"107","author":"Fauconnier","year":"2010","journal-title":"Proc. Natl. Acad. Sci. USA"},{"key":"ref_53","doi-asserted-by":"crossref","first-page":"H846","DOI":"10.1152\/ajpheart.00688.2006","article-title":"Intracellular calcium handling in ventricular myocytes from mdx mice","volume":"292","author":"Williams","year":"2007","journal-title":"Am. J. Physiol. Heart Circ. Physiol."},{"key":"ref_54","doi-asserted-by":"crossref","first-page":"177","DOI":"10.1016\/j.yjmcc.2015.11.009","article-title":"Crosstalk between RyR2 oxidation and phosphorylation contributes to cardiac dysfunction in mice with Duchenne muscular dystrophy","volume":"89","author":"Wang","year":"2015","journal-title":"J. Mol. Cell Cardiol."},{"key":"ref_55","doi-asserted-by":"crossref","unstructured":"Zullo, A., Frisso, G., and Carsana, A. (2019). Influence of physical activity on structure and function of the RyR1 calcium channel: A systematic review. Gazz. Med. Ital. Arch. Sci. Med., in press.","DOI":"10.23736\/S0393-3660.19.04238-4"},{"key":"ref_56","doi-asserted-by":"crossref","first-page":"C1502","DOI":"10.1152\/ajpcell.00435.2001","article-title":"Regulation of the cardiac L-type Ca2+ channel by the actin-binding proteins alpha-actinin and dystrophin","volume":"282","author":"Sadeghi","year":"2002","journal-title":"Am. J. Physiol. Cell Physiol."},{"key":"ref_57","doi-asserted-by":"crossref","first-page":"1205","DOI":"10.1096\/fj.01-0855com","article-title":"The carboxyl-terminal region of ahnak provides a link between cardiac L-type Ca2+ channels and the actin-based cytoskeleton","volume":"16","author":"Hohaus","year":"2002","journal-title":"FASEB J."},{"key":"ref_58","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1111\/j.1469-7793.2001.00363.x","article-title":"Cytochalasin D reduces Ca2+ currents via cofilin-activated depolymerization of F-actin in guinea-pig cardiomyocytes","volume":"537","author":"Rueckschloss","year":"2001","journal-title":"J. Physiol."},{"key":"ref_59","doi-asserted-by":"crossref","first-page":"H564","DOI":"10.1152\/ajpheart.00441.2013","article-title":"Enhanced Currents through L-Type Calcium Channels in Cardiomyocytes Disturb the Electrophysiology of the Dystrophic Heart","volume":"306","author":"Koenig","year":"2014","journal-title":"Am. J. Physiol. Heart Circ. Physiol."},{"key":"ref_60","doi-asserted-by":"crossref","unstructured":"Koenig, X., Dysek, S., Kimbacher, S., Mike, A.K., Cervenka, R., Lukacs, P., Nagl, K., Dang, X.B., Todt, H., and Bittner, R.E. (2011). Voltage-gated ion channel dysfunction precedes cardiomyopathy development in the dystrophic heart. PLoS ONE, 6.","DOI":"10.1371\/journal.pone.0020300"},{"key":"ref_61","doi-asserted-by":"crossref","first-page":"e13567","DOI":"10.14814\/phy2.13567","article-title":"Calcium Current Properties in Dystrophin-deficient Ventricular Cardiomyocytes from Aged Mdx Mice","volume":"6","author":"Rubi","year":"2018","journal-title":"Physiol. Rep."},{"key":"ref_62","doi-asserted-by":"crossref","first-page":"60","DOI":"10.1093\/cvr\/cvu119","article-title":"Blunted Cardiac Beta-Adrenergic Response as an Early Indication of Cardiac Dysfunction in Duchenne Muscular Dystrophy","volume":"103","author":"Li","year":"2014","journal-title":"Cardiovasc. Res."},{"key":"ref_63","doi-asserted-by":"crossref","first-page":"15118","DOI":"10.1038\/s41598-017-15087-0","article-title":"Identification of a novel cAMP dependent protein kinase A phosphorylation site on the human cardiac calcium channel","volume":"7","author":"Muralidharan","year":"2017","journal-title":"Sci. Rep."},{"key":"ref_64","doi-asserted-by":"crossref","first-page":"46","DOI":"10.1111\/1440-1681.12750","article-title":"The Cardiac L-Type Calcium Channel AlphaSubunit Is a Target for Direct Redox Modification during Oxidative Stress-the Role of Cysteine Residues in the Alpha Interacting Domain","volume":"44","author":"Muralidharan","year":"2017","journal-title":"Clin. Exp. Pharmacol. Physiol."},{"key":"ref_65","doi-asserted-by":"crossref","unstructured":"Koenig, X., Ebner, J., and Hilber, K. (2018). Voltage-Dependent Sarcolemmal Ion Channel Abnormalities in the Dystrophin-Deficient Heart. Int. J. Mol. Sci., 19.","DOI":"10.3390\/ijms19113296"},{"key":"ref_66","doi-asserted-by":"crossref","first-page":"1213","DOI":"10.1139\/cjpp-2017-0265","article-title":"Na+-H+ exchanger and proton channel in heart failure associated with Becker and Duchenne muscular dystrophies","volume":"95","author":"Bkaily","year":"2017","journal-title":"Can. J. Physiol. Pharmacol."},{"key":"ref_67","doi-asserted-by":"crossref","first-page":"139","DOI":"10.1016\/0306-9877(92)90087-S","article-title":"The dystrophin connection\u2014ATP?","volume":"38","author":"Bonsett","year":"1992","journal-title":"Med. Hypotheses"}],"container-title":["Journal of Clinical Medicine"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.mdpi.com\/2077-0383\/8\/12\/2151\/pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T13:40:29Z","timestamp":1760190029000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.mdpi.com\/2077-0383\/8\/12\/2151"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2019,12,5]]},"references-count":67,"journal-issue":{"issue":"12","published-online":{"date-parts":[[2019,12]]}},"alternative-id":["jcm8122151"],"URL":"https:\/\/doi.org\/10.3390\/jcm8122151","relation":{},"ISSN":["2077-0383"],"issn-type":[{"value":"2077-0383","type":"electronic"}],"subject":[],"published":{"date-parts":[[2019,12,5]]}}}