Heart Failure ; prevention & control ; Humans ; Mitochondria

Heart failure (HF) is a multifactorial disease brought about by numerous, and oftentimes complex, etiological mechanisms. Although well studied, HF continues to affect millions of people worldwide and current treatments can only prevent further progression of HF. Mitochondria undoubtedly play an important role in the progression of HF, and numerous studies have highlighted mitochondrial components that contribute to HF. This review presents an overview of the role of mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial permeability transition pore in HF, discusses ongoing studies that attempt to address the disease through mitochondrial targeting, and provides an insight on how these studies can affect future research on HF treatment.
Heart Failure* ; Heart* ; Mitochondria ; Organelle Biogenesis ; Oxidative Stress ; Permeability ; Protein Processing, Post-Translational

Acute myocardial infarction is one of the major causes of mortality worldwide. Reperfusion in a timely fashion is the most effective way to limit infarct size. However, reperfusion can itself prompt further myocardial injury. This phenomenon is commonly known as myocardial ischemia-reperfusion (IR) injury. Mitochondrial aldehyde dehydrogenase (ALDH2) is an enzyme metabolizing acetaldehyde and toxic aldehydes. Increasing evidence has revealed a cardioprotective role of ALDH2 in myocardial IR injury. Evidence from animal studies has shown that ALDH2 diminishes acute myocardial infarct size, ameliorates cardiac dysfunction and prevents reperfusion arrhythmias. The activity of ALDH2 is severely compromised if it is encoded by the mutant ALDH2*2 gene, with an incidence of approximately 40% in Asian populations. Epidemiological surveys in the Asian population have depicted that ALDH2 polymorphism is closely associated with higher prevalence of acute myocardial infarction and coronary artery disease. Therefore, targeting ALDH2 may represent a promising avenue to protect against IR injury. This review recapitulates the underlying mechanisms involved in the protective effect of ALDH2 in cardiac IR injury. Translational potential of ALDH2 in the management of coronary heart disease is also discussed.
Aldehyde Dehydrogenase ; metabolism ; Animals ; Heart ; physiopathology ; Humans ; Mitochondria, Heart ; enzymology ; Myocardial Reperfusion Injury ; Myocardium ; pathology

Mitochondria are subcellular organelles that provide energy for the cell. They form a dynamic tubular network and play an important role in maintaining the cell function and integrity. Heart is a powerful organ that supplies the motivation for circulation, thereby requiring large amounts of energy. Thus, the healthiness of cardiomyocytes and mitochondria is necessary for the normal cardiac function. Mitochondria not only lie in the center of the cell apoptotic pathway, but also are the major source of reactive oxygen species (ROS) generation. Mitochondrial morphological change includes fission and fusion that are regulated by a large number of proteins. In this review we discuss the regulators of mitochondrial fission/fusion and their association with cell apoptosis, autophagy and ROS production in the heart.
Animals ; Apoptosis ; Heart ; Humans ; Mitochondria, Heart ; metabolism ; Myocardium ; cytology ; metabolism ; Reactive Oxygen Species ; metabolism

Coenzyme Q is concentrated in Golgi apparatus membranes and mitochondria, but not in other membranes. Although it is difficult to prove the metabolic action of coenzyme Q administered exogenously in clinical cases, the effect of this substance can be evaluated by criteria based on clinical findings. In an attempt to evaluate the effect of coenzyme Q for the treatment of 67 patients(male 26 cases, female 41 cases) of congestive heart failure, we administered Coenzyme Q1030mg daily for 4 to 8 weeks. Most of them were valvular heart disease(74.6%) and hypertension (14.9%). Clinical effects were evaluated at least 4 weeks later by the criteria using a scoring method of severity of congestive heart failure which was devised by Ishiyama, etc. In summary, a definite effect was found in 13 cases(19%) and a mild effect was observed in 46 cases(69%). During treatment there were no significant side effects, and also no significant changes in heart rate and blood pressure.
Blood Pressure ; Estrogens, Conjugated (USP)* ; Female ; Golgi Apparatus ; Heart ; Heart Failure* ; Heart Rate ; Humans ; Hypertension ; Membranes ; Mitochondria ; Research Design ; Ubiquinone

No abstract available.
Mitochondria, Heart ; Gasotransmitters ; Adenosine Diphosphate ; Myocardial Reperfusion Injury ; Cardiotonic Agents ; Electron Transport Complex IV

Adenosine Triphosphate ; pharmacology ; Animals ; Burns ; metabolism ; Calcium ; metabolism ; Female ; Male ; Mitochondria, Heart ; metabolism ; Rats

Burns ; complications ; pathology ; physiopathology ; Humans ; Mitochondria, Heart ; pathology ; Myocardial Ischemia ; etiology ; prevention & control

As the final destination of various cardiovascular abnormalities, heart failure is one of the diseases with the highest morbidity and mortality in the world. Due to its complicated pathogenesis, people urgently need to find new targets and effective treatment. Imbalance in myocardial energy metabolism, an important molecular biological basis for heart failure, affects the contractile and diastolic functions of the heart. As the main source of energy synthesis in cardiomyocytes and an important participant in various signaling pathways, mitochondria plays an indispensable role in the process of cell survival and death and has been considered as a critical target for the treatment of heart failure. Traditional Chinese medicine has a great effect on the treatment of heart failure through multi-components, multi-targets, and multi-channels. In recent years, more and more researches regard mitochondria as the target of traditional Chinese medicine in the treatment of heart failure, and have achieved significant results in improving mitochondrial function, increasing energy metabolism and energy supplement for cardiomyocytes, and resisting against oxidative stress. In this article, researches on the regulation of mitochondria in the treatment of heart failure by traditional Chinese medicine are reviewed from four aspects: mitochondrial biogenesis; mitochondrial electron transport chain and reactive oxygen species(ROS) production; metabolic substrates and metabolic enzymes; and calcium ion transport in the mitochondria. It provides a basis for further research and clinical application in the future.
Heart Failure ; Humans ; Medicine, Chinese Traditional ; Mitochondria ; Oxidative Stress ; Reactive Oxygen Species

Cardiac hypertrophy is a common pathological process of various cardiovascular diseases and eventually develops into heart failure. This paper was aimed to study the different pathological characteristics exhibited by different mouse strains after hypertrophy stimulation. Two mouse strains, A/J and FVB/nJ, were treated with isoproterenol (ISO) by osmotic pump to induce cardiac hypertrophy. Echocardiography was performed to monitor heart morphology and function. Mitochondria were isolated from hearts in each group, and oxidative phosphorylation function was assayed in vitro. The results showed that both strains showed a compensatory enhancement of heart contractile function after 1-week ISO treatment. The A/J mice, but not the FVB/nJ mice, developed significant cardiac hypertrophy after 3-week ISO treatment as evidenced by increases in left ventricular posterior wall thickness, heart weight/body weight ratio, cross sectional area of cardiomyocytes and cardiac hypertrophic markers. Interestingly, the heart from A/J mice contained higher mitochondrial DNA copy number compared with that from FVB/nJ mice. Functionally, the mitochondria from A/J mice displayed faster O
Animals ; Cardiomegaly/chemically induced* ; Heart Failure ; Isoproterenol/toxicity* ; Mice ; Mitochondria ; Myocytes, Cardiac/metabolism*