دورية أكاديمية

Short Communication: Ischemia/Reperfusion Tolerance Is Time-of-Day–Dependent ; Mediation by the Cardiomyocyte Circadian Clock

التفاصيل البيبلوغرافية
العنوان: Short Communication: Ischemia/Reperfusion Tolerance Is Time-of-Day–Dependent ; Mediation by the Cardiomyocyte Circadian Clock
المؤلفون: Durgan, David J., Pulinilkunnil, Thomas, Villegas-Montoya, Carolina, Garvey, Merissa E., Frangogiannis, Nikolaos G., Michael, Lloyd H., Chow, Chi-Wing, Dyck, Jason R.B., Young, Martin E.
المصدر: Circulation Research ; volume 106, issue 3, page 546-550 ; ISSN 0009-7330 1524-4571
بيانات النشر: Ovid Technologies (Wolters Kluwer Health)
سنة النشر: 2010
الوصف: Rationale : Cardiovascular physiology and pathophysiology vary dramatically over the course of the day. For example, myocardial infarction onset occurs with greater incidence during the early morning hours in humans. However, whether myocardial infarction tolerance exhibits a time-of-day dependence is unknown. Objective : To investigate whether time of day of an ischemic insult influences clinically relevant outcomes in mice. Methods and Results : Wild-type mice were subjected to ischemia/reperfusion (I/R) (45 minutes of ischemia followed by 1 day or 1 month of reperfusion) at distinct times of the day, using the closed-chest left anterior descending coronary artery occlusion model. Following 1 day of reperfusion, hearts subjected to ischemia at the sleep-to-wake transition (zeitgeber time [ZT]12) resulted in 3.5-fold increases in infarct size compared to hearts subjected to ischemia at the wake-to-sleep transition (ZT0). Following 1 month of reperfusion, prior ischemic event at ZT12 versus ZT0 resulted in significantly greater infarct volume, fibrosis, and adverse remodeling, as well as greater depression of contractile function. Genetic ablation of the cardiomyocyte circadian clock (termed cardiomyocyte-specific circadian clock mutant [CCM] mice) attenuated/abolished time-of-day variations in I/R outcomes observed in wild-type hearts. Investigation of Akt and glycogen synthase kinase-3β in wild-type and CCM hearts identified these kinases as potential mechanistic ties between the cardiomyocyte circadian clock and I/R tolerance. Conclusions : We expose a profound time-of-day dependence for I/R tolerance, which is mediated by the cardiomyocyte circadian clock. Further understanding of I/R tolerance rhythms will potentially provide novel insight regarding the etiology and treatment of ischemia-induced cardiac dysfunction.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1161/circresaha.109.209346
DOI: 10.1161/CIRCRESAHA.109.209346
الإتاحة: https://doi.org/10.1161/circresaha.109.209346Test
رقم الانضمام: edsbas.FA1AF543
قاعدة البيانات: BASE