It is important to establish successfully animal models in the study of pathogenesis,diagnosis and treatment of heart failure.This article reviewe drecent animal models of heart failure.

Atherosclerosis is a multifactorial disease for which the molecular etiology of many of the risk factors is still unknown.Reactive oxygen species(ROS) mediate various signaling pathways that underlie vascular inflammation in atherogenesis: from the initiation of fatty streak development through lesion progress to ultimate plaque rupture.The mitochondrial respiratory chain is the major source of reactive oxygen species as byproducts of normal cell respiration.Mitochondria may also be important target for reactive oxygen species,which may lead to mitochondrial dysfunction.Moreover,in patients with mitochondrial diseases,vascular complications are commonly observed at an early age,often in the absence of traditional risk factors for atherosclerosis.The aim of this review is to summarize the data linking mitochondrial dysfunction to the pathogenesis of atherosclerosis.

Intracoronary stent implantation is a safe and effective treatment for coronary artery disease.In-stent restenosis has been significantly reduced by utilization of drug eluting stents.This article reviews the results of long-term follow-up after intracoronary stent implantation and their implication.

The glucose transporter(GLUT) is an energy-related carrier protein located on the cell membrane.Most researches have shown that changes of energy metabolism play an important role in the development of heart failure.This review summarizes recent advances in the understanding of the relationship between GLUT and heart failure.

Angina pectoris is an important event in coronary heart disease.Many researches are conducted on the risk factors and risk stratification of the problem,so as to classify the patients into different risk groups,properly predict their prognosis,take the most effective therapeutic measures and achieve the best results with the least risks and expenses.

It is very important to successfully establish stable and reliable animal models in the study of pathogenesis,pathophysiology,prevention and treatment of heart failure.Although the establishment,maintenance and a long time observation of right heart failure animal models are difficult,they have great clinical values.This article reviews the recent study about modeling methods,animal choice and modeling mechanisms of animal models of right heart failure.

Diabetic cardiomyopathy is one of the main causes of death in diabetic patients.Mitochondrial dysfunction plays a key role in the development of diabetic cardiomyopathy,and mitochondrial function depends on the stabilization of the mitochondrial membrane structure.Studies on the molecular alteration and the underlying mechanism of the cardiocyte mitochondrial membrane of the diabetic heart may give us deeper insights into diabetic cardiomyopathy,and help us make a breakthrough in the therapeutic strategies.

Objective Diabetic mellitus is one of the major threats to human health.The prevalence of diabetes mellitus is growing rapidly worldwide.Patients with diabetes mellitus are at increased risk for cardiovascular diseases.Diabetic cardiomyopathy (DC) is related to diabetes-specific metabolism,but the mechanism is not entirely clear.Recent studies suggest that abnormal myocardial energy metabolism and reduced number of myocardial cells may be the important pathophysiological mechanism that leads to heart function impairment of diabetes patients.Mitochondria are not only an important place generating cellular energy,also involved in the apoptotic and death process of cells.Therefore,mitochondrial dysfunctions play a key role in the process of DC.Mitochondrial permeability transition (MPT) is a center for information exchange within and outside the mitochondria and plays a key role in the maintenance of mitochondrial function.MPT works through the mitochondrial permeability transition pore (MPTP).In our recent studies,it was found that MPTP function changed in DC and its abnormality could be corrected by specific AT I receptor antagonist.These findings are important for better understanding DC.

Human recombinant B type natriuretic peptide(hBNP) binds to receptor in the vasculature, kidney, and other organs to mimic the action of endogenous natriuretic peptides. Intravenous infusion of hBNP has been studied with acute decompensated heart failure. It causes potent, dose related vasodilation that is rapid in onset and sustained for the duration of drug infusion, reflected by decreases in systemic vascular resistance, systemic arterial pressure, pulmonary capillary wedge pressure, right atrial pressure, and mean pulmonary arterial pressure. Vasodilation occurs without a change in heart rate and is associated with increases in stroke volume and cardiac output. hBNP may promote diuresis because of a direct natriuretic action, increased cardiac output, and decreased aldosterone levels. For decompensated heart failure, hBNP improves symptoms and is well tolerated. The major adverse effect is dose related hypotension. As a new vasodilator, it should be valuable in treatment of patients hospitalized for decompensated heart failure.

Brain natriuretic peptide(BNP) emerges as another cardiac hormone after atrial natriuretic peptide (ANP). It plays a prominent role in natriuresis, diuresis, vasorelaxation and decreasing blood pressure. The plasma levels of BNP are closely related to the left ventricular function. In this review, the author highlights the latest progress of BNP in the diagnosis, risk stratification, prognosis and therapeutic monitoring of patients with congestive heart failure and other cardiac dysfunction.