Mitochondrial function in cardiac hypertrophy

2013 ◽  
Vol 167 (4) ◽  
pp. 1118-1125 ◽  
Author(s):  
Lu-Yu Zhou ◽  
Jin-Ping Liu ◽  
Kun Wang ◽  
Jie Gao ◽  
Su-Ling Ding ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Mitochondrial Function

scholarly journals Overexpression of the Serotonin 5-HT 2B Receptor in Heart Leads to Abnormal Mitochondrial Function and Cardiac Hypertrophy

Circulation ◽  
2003 ◽  
Vol 107 (25) ◽  
pp. 3223-3229 ◽  
Author(s):  
Canan G. Nebigil ◽  
Fabrice Jaffré ◽  
Nadia Messaddeq ◽  
Pierre Hickel ◽  
Laurent Monassier ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Mitochondrial Function

scholarly journals Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function

Nature ◽  
2011 ◽  
Vol 478 (7367) ◽  
pp. 114-118 ◽  
Author(s):  
Chris McDermott-Roe ◽  
Junmei Ye ◽  
Rizwan Ahmed ◽  
Xi-Ming Sun ◽  
Anna Serafín ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Mitochondrial Function ◽  
Endonuclease G

scholarly journals Overexpression of miR-142-3p improves mitochondrial function in cardiac hypertrophy

2018 ◽  
Vol 108 ◽  
pp. 1347-1356 ◽  
Author(s):  
Bei-lei Liu ◽  
Mian Cheng ◽  
Shan Hu ◽  
Shun Wang ◽  
Le Wang ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Mitochondrial Function

scholarly journals Calorie Restriction Maintains Mitochondrial Function and Redox Balance Avoiding Lipidomic Reprogramming during Isoproterenol-Induced Cardiac Hypertrophy

2021 ◽  
Author(s):  
Cícera Edna Barbosa David ◽  
Aline Maria Brito Lucas ◽  
Pedro Lourenzo Oliveira Cunha ◽  
Yuana Ivia Ponte Viana ◽  
Marcos Yukio Yoshinaga ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cardiac Hypertrophy ◽  
Calorie Restriction ◽  
Mitochondrial Function ◽  
Cardiac Tissue ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Respiratory Control ◽  
H2o2 Production

Cardiac hypertrophy induces a metabolic shift, leading to a preferential consumption of glucose (over fatty acids) to support the high energetic demand. Typically, health cardiac tissue utilizes more fat than any other organ. Calorie restriction is a dietary procedure that induces health benefits and lifespan extension in many organisms. Given the beneficial effects of calorie restriction and the metabolic dysregulation seen during cardiac hypertrophy, we hypothesized that calorie restriction prevents cardiac hypertrophy, lipid, mitochondrial, and redox dysregulations. Strikingly, calorie restriction reversed isoproterenol-induced cardiac hypertrophy, lowered succinate driven mitochondrial H2O2 production, improved mitochondrial function (indicated as a higher Respiratory Control Ratio – RCR) and avoided mitochondrial superoxide dismutase (MnSOD) and glutathione peroxidase (GPX) repression. To gain insight into how calorie restriction could interfere with the metabolic changes induced by cardiac hypertrophy, we performed lipidomic profiling. Calorie restriction protected against the consumption of several triglycerides (TG) linked to unsaturated fatty acids, and the accumulation of TGs containing saturated fatty acids observed in hypertrophic samples. Cardiac hypertrophy induced an increase in ceramides, phosphoethanolamines and acylcarnitines (12:0, 14:0, 16:0 and 18:0) that were also reversed by calorie restriction. Altogether, our data demonstrate that hypertrophy changes the cardiac lipidome, causes mitochondrial disturbances and oxidative stress. All these changes are prevented by calorie restriction intervention in vivo. This study uncovers calorie restriction as a resource protect cardiac tissue and prevent cardiac hypertrophy-induced lipidomic remodeling.

scholarly journals Overexpression of NOX2 Exacerbates AngII-Mediated Cardiac Dysfunction and Metabolic Remodelling

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 143
Author(s):  
Synne S. Hansen ◽  
Tina M. Pedersen ◽  
Julie Marin ◽  
Neoma T. Boardman ◽  
Ajay M. Shah ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Mitochondrial Function ◽  
Cardiac Dysfunction ◽  
Mechanical Efficiency ◽  
Substrate Utilization ◽  
Low Doses ◽  
Myocardial Substrate

The present study aimed to examine the effects of low doses of angiotensin II (AngII) on cardiac function, myocardial substrate utilization, energetics, and mitochondrial function in C57Bl/6J mice and in a transgenic mouse model with cardiomyocyte specific upregulation of NOX2 (csNOX2 TG). Mice were treated with saline (sham), 50 or 400 ng/kg/min of AngII (AngII50 and AngII400) for two weeks. In vivo blood pressure and cardiac function were measured using plethysmography and echocardiography, respectively. Ex vivo cardiac function, mechanical efficiency, and myocardial substrate utilization were assessed in isolated perfused working hearts, and mitochondrial function was measured in left ventricular homogenates. AngII50 caused reduced mechanical efficiency despite having no effect on cardiac hypertrophy, function, or substrate utilization. AngII400 slightly increased systemic blood pressure and induced cardiac hypertrophy with no effect on cardiac function, efficiency, or substrate utilization. In csNOX2 TG mice, AngII400 induced cardiac hypertrophy and in vivo cardiac dysfunction. This was associated with a switch towards increased myocardial glucose oxidation and impaired mitochondrial oxygen consumption rates. Low doses of AngII may transiently impair cardiac efficiency, preceding the development of hypertrophy induced at higher doses. NOX2 overexpression exacerbates the AngII -induced pathology, with cardiac dysfunction and myocardial metabolic remodelling.

Alterations in mitochondrial function in cardiac hypertrophy and heart failure

2012 ◽  
Vol 18 (5) ◽  
pp. 645-656 ◽  
Author(s):  
Moritz Osterholt ◽  
T. Dung Nguyen ◽  
Michael Schwarzer ◽  
Torsten Doenst
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Mitochondrial Function

scholarly journals Hispidulin Attenuates Cardiac Hypertrophy by Improving Mitochondrial Dysfunction

2020 ◽  
Vol 7 ◽  
Author(s):  
Yan Wang ◽  
Zengshuo Xie ◽  
Nan Jiang ◽  
Zexuan Wu ◽  
Ruicong Xue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Mitochondrial Function ◽  
Specific Inhibitor ◽  
Cardiomyocyte Hypertrophy ◽  
Mitochondrial Morphology ◽  
Protective Effects

Cardiac hypertrophy is a pathophysiological response to harmful stimuli. The continued presence of cardiac hypertrophy will ultimately develop into heart failure. The mitochondrion is the primary organelle of energy production, and its dysfunction plays a crucial role in the progressive development of heart failure from cardiac hypertrophy. Hispidulin, a natural flavonoid, has been substantiated to improve energy metabolism and inhibit oxidative stress. However, how hispidulin regulates cardiac hypertrophy and its underlying mechanism remains unknown. We found that hispidulin significantly inhibited pressure overload-induced cardiac hypertrophy and improved cardiac function in vivo and blocked phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. We further proved that hispidulin remarkably improved mitochondrial function, manifested by increased electron transport chain (ETC) subunits expression, elevated ATP production, increased oxygen consumption rates (OCR), normalized mitochondrial morphology, and reduced oxidative stress. Furthermore, we discovered that Sirt1, a well-recognized regulator of mitochondrial function, might be a target of hispidulin, as evidenced by its upregulation after hispidulin treatment. Cotreatment with EX527 (a Sirt1-specific inhibitor) and hispidulin nearly completely abolished the antihypertrophic and protective effects of hispidulin on mitochondrial function, providing further evidence that Sirt1 could be the pivotal downstream effector of hispidulin in regulating cardiac hypertrophy.

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