title: Calcium signaling in diabetic cardiomyocytes.
abstract: Diabetes mellitus is one of the most common medical conditions. It is associated to medical complications in numerous organs and tissues, of which the heart is one of the most important and most prevalent organs affected by this disease. In fact, cardiovascular complications are the most common cause of death among diabetic patients. At the end of the 19th century, the weakness of the heart in diabetes was noted as part of the general muscular weakness that exists in that disease. However, it was only in the eighties that diabetic cardiomyopathy was recognized, which comprises structural and functional abnormalities in the myocardium in diabetic patients even in the absence of coronary artery disease or hypertension. This disorder has been associated with both type 1 and type 2 diabetes, and is characterized by early-onset diastolic dysfunction and late-onset systolic dysfunction, in which alteration in Ca(2+) signaling is of major importance, since it controls not only contraction, but also excitability (and therefore is involved in rhythmic disorder), enzymatic activity, and gene transcription. Here we attempt to give a brief overview of Ca(2+) fluxes alteration reported on diabetes, and provide some new data on differential modulation of Ca(2+) handling alteration in males and females type 2 diabetic mice to promote further research. Due to space limitations, we apologize for those authors whose important work is not cited.
authors.affiliation: Department of Pharmacology, University of California Davis, Davis, CA 95616, USA.
authors.forename: Laetitia
authors.initials: L
authors.lastname: Pereira
authors.affiliation: Unidad de Hipertensión, Instituto de Investigación i+12, Hospital Universitario 12 de Octubre, Madrid, Spain; Instituto Pluridisciplinar, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.
authors.forename: Gema
authors.initials: G
authors.lastname: Ruiz-Hurtado
authors.affiliation: Departamento de Bioquímica, Cinvestav-IPN, México, DF, Mexico.
authors.forename: Angélica
authors.initials: A
authors.lastname: Rueda
authors.affiliation: Inserm, UMR S769, Faculté de Pharmacie, Université Paris Sud, Labex LERMIT, DHU TORINO, Châtenay-Malabry, France; Université Paris Diderot - Sorbonne Paris Cité, Assistance Publique - Hôpitaux de Paris (AP-HP), France.
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Mercadier
authors.affiliation: Inserm, UMR S769, Faculté de Pharmacie, Université Paris Sud, Labex LERMIT, DHU TORINO, Châtenay-Malabry, France.
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Benitah
authors.affiliation: Inserm, UMR S769, Faculté de Pharmacie, Université Paris Sud, Labex LERMIT, DHU TORINO, Châtenay-Malabry, France. Electronic address: ana-maria.gomez@inserm.fr.
authors.forename: Ana María
authors.initials: AM
authors.lastname: Gómez
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000235:genetics*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D058065:Diabetic Cardiomyopathies / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000235:genetics; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012727:Sex Characteristics
chemical_list: D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium
keywords: Calcium; Calcium sparks; Diabetes; Ryanodine receptors; Sex related differences