Complex Regulation of Mitochondrial Function During Cardiac Development

Zhao, Qiancong; Sun, Qianchuang; Zhou, Lufang; Liu, Kexiang; Jiao, Kai

doi:10.1161/jaha.119.012731

Cited by 70 publications

(79 citation statements)

References 155 publications

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“…Also, the heart needs the energy to maintain its normal function. Mitochondrial organelle is one of the most important sources of energy production [14][15][16]. Therefore, mitochondrial dysfunction in the heart may have irreparable consequences.…”

Section: Discussionmentioning

confidence: 99%

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Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

2020

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Propranolol and atenolol are known as β receptor blocker drugs. These drugs are used to treat some heart diseases. There are controversies in the relationship between the use of beta-blocker drugs and the level of reactive oxygen species (ROS). Mitochondria as one of the most important sources of ROS are considered as one of the targets of drug-induced cardiotoxicity. The aim of this study was to evaluate the effects of propranolol and atenolol on mitochondria isolated from the heart. To achieve this aim, several markers of mitochondrial and cellular toxicity were evaluated. The key results of this study are the increased ROS level, collapse in mitochondrial membrane potential (MMP), mitochondrial swelling and cytochrome c release as well as disruption of respiratory chain complex II in mitochondria in isolated heart mitochondria after exposure to propranolol and atenolol. The results indicate an increase in caspase-3 activity and a decrease in the ATP level in cardiomyocytes after exposure to propranolol and atenolol. The underlying mechanisms of propranolol and atenolol induced cardiotoxicity may be associated with alterations in mitochondrial function, oxidative stress, and changes in the mitochondrial membrane.

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Section: Discussionmentioning

confidence: 99%

“…The heart needs the energy to maintain its normal function. Mitochondrial organelle is one of the most important sources of energy production [14][15][16]. In addition to supplying energy to cells, mitochondria are known to be one of the most important sources of ROS generation in the cell as well as cell death.…”

Section: Introductionmentioning

confidence: 99%

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

2020

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“…Multiple other disease states are associated with cardiac mitochondrial superstructure changes, such as alcohol-induced heart failure [32,33], cardiac hypertrophy [34], cardiovascular reperfusion injury [35], congenital heart diseases [36], heart failure [37], myocardial infarction [38], and myocardial ischemia-reperfusion injury [39]. In this study, we showed that burn-induced heart dysfunction is associated with cardiac mitochondrial morphological damage.…”

Section: Discussionmentioning

confidence: 58%

Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway

Wen

Cummins

Radhakrishnan

2020

IJMS

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Burn-induced heart dysfunction is a key factor for patient mortality. However, the molecular mechanisms are not yet fully elucidated. This study sought to understand whether burn-induced heart dysfunction is associated with cardiac mitochondrial dysfunction and interruption of the PDE5A-cGMP-PKG pathway. Sixty percent total body surface area (TBSA) scald burned rats (±sildenafil) were used in this study. A transmission electron microscope (TEM), real-time qPCR, O2K-respirometer, and electron transport chain assays were used to characterized molecular function. Cardiac mitochondrial morphological shapes were disfigured with a decline in mitochondrial number, area, and size, resulting in deficiency of cardiac mitochondrial replication. Burn induced a decrease in all mitDNA encoded genes. State 3 oxygen consumption was significantly decreased. Mitochondrial complex I substrate-energized or complex II substrate-energized and both of respiratory control ratio (RCRs) were decreased after burn. All mitochondrial complex activity except complex II were decreased in the burn group, correlating with decreases in mitochondrial ATP and MnSOD activity. Sildenafil, a inhibitor of the PDE5A-cGMP-PKG pathway, preserved the mitochondrial structure, respiratory chain efficiency and energy status in cardiac tissue. Furthermore, sildenafil treatment significantly restored ADP-conjugated respiration in burned groups. In conclusion, cardiac mitochondrial damage contributes to burn-induced heart dysfunction via the PDE5A-cGMP-PKG pathway.

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“…In addition, energy consumption in the heart is similar to that of the brain. On the other hand, the heart needs energy for its normal function and development, and mitochondria are the source of this energy [16,35,36].…”

Section: Discussionmentioning

confidence: 99%

“…Many compounds have caused mitochondrial toxicity and these organelles has become one of the research targets [13,14]. Brain and heart tissues depend on mitochondria for their high energy consumption and maintenance of their normal function [15,16]. Research has shown that mitochondria are one of the targets of PPARγ agonists [3,17,18].…”

Section: Introductionmentioning

confidence: 99%

Toxicity of Pioglitazone on Mitochondria Isolated from Brain and Heart: An Analysis for Probable Drug-Induced Neurotoxicity and Cardiotoxicity

et al. 2020

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Pioglitazone (PG) is one of the thiazolidinedione (TZDs) drugs used in diabetic patients. TZDs are known as peroxisome proliferator-activated receptor gamma (PPARγ) agonists. Mitochondria are considered as one of the targets of these drugs. The mechanisms of the effect of PG on mitochondria are not well understood. In this study, we investigated the effect of PG on mitochondria isolated from brain and heart. Mitochondrial parameters such as succinate dehydrogenase (SDH) activity, reactive oxygen species (ROS) generation, collapse in mitochondrial membrane potential (MMP), mitochondrial swelling and cytochrome c release were evaluated. The results showed that PG at concentrations of 12.5, 25 and 50 µg/ml increased the generation of ROS, the collapse of MMP, mitochondrial swelling and the release of cytochrome c in mitochondria isolated from both brain and heart tissues. The underlying mechanisms of PG induced neuro-toxicity and cardio-toxicity may be associated with changes in mitochondrial function, ROS generation (oxidative stress), and changes in the mitochondrial membrane.

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Complex Regulation of Mitochondrial Function During Cardiac Development

Cited by 70 publications

References 155 publications

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway

Toxicity of Pioglitazone on Mitochondria Isolated from Brain and Heart: An Analysis for Probable Drug-Induced Neurotoxicity and Cardiotoxicity

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