Heart Failure ; prevention & control ; Humans ; Mitochondria

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

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

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

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

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

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*

Traditionally, mitochondria have been regarded solely as energy generators for cells; however, accumulating data have demonstrated that these complex organelles play a variety of roles within the cardiomyocyte that extend beyond this classic function. Mitochondrial dynamics involves mitochondrial movements and morphologic alterations by tethering, fusion, and fission, which depend on cellular energy requirements and metabolic status. Many studies have indicated that mitochondrial dynamics may be a fundamental component of the maintenance of normal cellular homeostasis and cardiac function. Mitochondrial dynamics is controlled by the protein machinery responsible for mitochondrial fusion and fission, but cardiomyocytes are densely packed as part of an intricate cytoarchitecture for efficient and imbalanced contraction; thus, mitochondrial dynamics in the adult heart are restricted and occur more slowly than in other organs. Cardiac mitochondrial dynamics is important for cardiac physiology in diseased conditions such as ischemia-reperfusion (IR) injury. Changes in mitochondrial morphology through modulation of the expression of proteins regulating mitochondrial dynamics demonstrates the beneficial effects on cardiac performance after IR injury. Thus, accurately defining the roles of mitochondrial dynamics in the adult heart can guide the identification and development of novel therapeutic targets for cardioprotection. Further studies should be performed to establish the exact mechanisms of mitochondrial dynamics.
Adult ; Heart ; Homeostasis ; Humans ; Mitochondria ; Mitochondrial Dynamics ; Myocardial Reperfusion Injury ; Myocytes, Cardiac ; Organelles ; Physiology