https://scholars.lib.ntu.edu.tw/handle/123456789/594682
Title: | Aldosterone suppresses cardiac mitochondria | Authors: | Hung, Chi-Sheng Chang, Yi-Yao CHENG-HSUAN TSAI Liao, Che-Wei Peng, Shih-Yuan BO-CHING LEE CHIEN-TING PAN Wu, Xue-Ming ZHENG-WEI CHEN Wu, Vin-Cent Wan, Cho-Hua Young, Morag J Chou, Chia-Hung Lin, Yen-Hung |
Issue Date: | Jan-2022 | Publisher: | Elsevier | Journal Volume: | 239 | Start page/Pages: | 58 | Source: | Translational research : the journal of laboratory and clinical medicine | Abstract: | Elevated serum aldosterone promotes arterial hypertension, cardiac hypertrophy, and diastolic dysfunction. However, the effect of elevated aldosterone levels on cardiac mitochondria remains unclear. We used primary cultures of mouse cardiomyocytes to determine whether aldosterone has direct effects on cardiomyocyte mitochondria, and aldosterone-infused mice as a preclinical model to evaluate the impact of aldosterone in vivo. We show that aldosterone suppressed mtDNA copy number and SOD2 expression via the mineralocorticoid receptor (MR)-dependent regulation of NADPH oxidase 2 (NOX2) and generation of reactive oxygen species (ROS) in primary mouse cardiomyocytes. Aldosterone suppressed cardiac mitochondria adenosine triphosphate production, which was rescued by N-acetylcysteine. Aldosterone infusion for 4 weeks in mice suppressed the number of cardiac mitochondria, mtDNA copy number, and SOD2 protein expression. MR blockade by eplerenone or the administration of N-acetylcysteine prevented aldosterone-induced cardiac mitochondrial damage in vivo. Similarly, patients with primary aldosteronism had a lower plasma leukocyte mtDNA copy number. Plasma leukocyte mtDNA copy number was positively correlated with 24-hour urinary aldosterone level and left ventricular mass index. In conclusion, aldosterone suppresses cardiac mitochondria in vivo and directly via MR activation of ROS pathways. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/594682 | ISSN: | 19315244 | DOI: | 10.1016/j.trsl.2021.08.003 |
Appears in Collections: | 醫學系 |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.