Ischemia heart disease is often accompanied by cardiac energy metabolism, which is reflected in contractile dysfunction and a decrease in cardiac efficiency. Specific metabolic changes include a relative increase in cardiac fatty acid oxidation rates and an uncoupling of glycolysis from glucose oxidation. Recent evidence suggests that therapeutically regulating cardiac energy metabolism by reducing fatty acid oxidation and/or increasing glucose oxidation can improve cardiac function of the ischemic heart. With the development of metabolomics technology, the detection methods and mechanisms of early metabolites for ischemic cardiomyopathy are further explored. This paper first discusses systematically the change of energy metabolic which contributes to cardiac dysfunction, and then it explores the potential for targeting treatment ischemic heart disease through metabolic pathway.
Cardiomyocytes, a kind of completely differentiated cells, are believed not to be able to proliferate. Recent studies indicate, however, that adult mammalian cardiomyocytes turn over at a certain rate. These studies use different approaches including isotype incorporation and genetic knock-in mice lineage tracing. Cardiomyocyte proliferation may be regulated by complicated molecular network as well as varied environment or microenvironment. Special characteristic features in cardiomyocytes themselves also have an impact on their proliferation.
Myocardial remodeling is an independent risk factor for major cardiovascular events such as heart failure. An abnormal increase in mechanical stress caused by hemodynamic pathological changes can directly trigger myocardial remodeling, accompanied by increased expression of neurohumoral factors, resulting in a synergistic effect which could further aggravate myocardial remodeling. Myocardial remodeling can be divided into pressure overload myocardial remodeling and volume overload myocardial remodeling, according to the type of mechanical stress overload. There are significant differences in the two types of myocardial remodeling at the gross structural, cellular, and molecular levels of the heart. Although volume overload is prevalent in various heart diseases, previous studies have focused on pressure overload myocardial remodeling, with a lack of sufficient elucidation of volume overload myocardial remodeling. It has been discovered through research that calcium-handling proteins and Akt may be held responsible for the difference between the two types of overload myocardial remodeling. This paper, which combines the previous achievements with our latest research results, outlines the similarities and differences between the two types of mechanical stress myocardial remodeling, attempts to shed some new light on precision research and personalized diagnosis and treatment of cardiac hypertrophy.
Vascular aging refers to the structural and functional changes of aorta during the aging process. It is characterized by vascular remodeling, vascular dyshomeostasis and vascular cell senescence. Epigenetic regulation can influence gene expression without changing the DNA sequence and it mainly includes DNA methylation, histone modifications, and RNA-based gene regulation. Current researches demonstrate that epigenetic regulation plays important roles in vascular aging and age-related diseases, and drugs targeting epigenetic regulation are expected to be new treatments for age-related diseases.
Cholesterol efflux, the first step in reverse cholesterol transport, is an important mechanism for maintaining cell homeostasis. Adenosine triphophate (ATP)-binding cassette (ABC) transporter G1 (ABCG1) maintains cellular cholesterol homeostasis by promoting intracellular cholesterol efflux to high density lipoprotein and it plays a crucial role in atherosclerosis, obesity and diabetes. The expression of ABCG1 is regulated by several factors, including transcript factor, protein modification, DNA methylation and microRNA, and subsequently it contributes to the development of several diseases. In this paper, the role of ABCG1 and its regulation in cardiovascular diseases have been reviewed, and it is hoped that exploration into this area will help bring about new ideas for the research in this field.
In-stent neoatherosclerosis (ISNA) has been identified as a major contributing factor to late stent failure resulting from stent thrombosis (ST) and in-stent restenosis (ISR). However, the accurate mechanism of ISNA remains unknown to this day and the absence of effective therapeutic strategy remains an essential issue to be solved. Hence, future studies should focus on the mechanism of ISNA progression and the treatment of ISNA, which are of great clinical significance for improving the prognosis of patients following stent implantation. In this paper, the basic and clinic advances of ISNA have been addressed.
Atherosclerosis is a complex chronic inflammatory disease involving multiple key pathological steps such as endothelial activation, endothelial dysfunction, and local inflammatory response. SUMOylation is a newly discovered post-translational modification in eukaryotic cells and is involved in a variety of cellular biological events such as cell proliferation and differentiation, apoptosis and cell signaling. Recent studies have found that SUMOylation is closely related to the development of atherosclerosis. This paper reviews the research status of the post-translational SUMOylation involved in the process of atherosclerosis and its mechanism.
Increasing evidence supports the protective role of exercise training in preventing cardiovascular diseases. Exercise induces physiological cardiac growth, and thus protects the heart against pathological remodeling and heart failure. Cardiac hypertrophy falls into two types, namely, the physiological cardiac hypertrophy and the pathological cardiac hypertrophy, and the latter can result in impaired cardiac functioning, heart failure and is predictive of a higher incidence of death due to cardiovascular diseases. Non-coding RNAs (ncRNAs) including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) have drawn significant attention over the last couple of decades, and their dysregulation is increasingly being linked to many cardiovascular diseases. In this paper, the profiling function, and molecular mechanism of miRNAs, lncRNAs, and circ- RNAs in cardiac hypertrophy, especially in physiological hypertrophy have been analyzed. Targeting these ncRNAs represents novel therapy for heart failure.
Loss of functional cardiomyocytes is a major contributing factor to myocardial remodeling and heart diseases due to limited regenerative capacity of adult myocardium. Apoptosis, programmed necrosis, and autophagy contribute to loss of cardiac myocytes that control the balance of cardiac cell death and cell survival through multiple intricate signaling pathways. In recent years, non-coding RNAs (ncRNAs) have received much attention because of their roles in cell death of cardiovascular diseases, such as myocardial infarction, cardiac hypertrophy, and heart failure. In addition, based on the view that mitochondrial morphology is linked to three types of cell death, ncRNAs are able to regulate mitochondrial fission/fusion of cardiomyocytes by targeting genes involved in cell death pathways. This paper focuses on recent progress regarding the complex relationship between apoptosis/necrosis/autophagy and ncRNAs in the context of myocardial cell death in response to stress. This paper also provides insight into the treatment for heart diseases that will guide novel therapies in the future.
