摘要：
N6-methyladenosine (m6A) is the most abundant and prevalent epigenetic modification of mRNA in mammals. This dynamic modification is regulated by m6A methyltransferases and demethylases, which control the fate of target mRNAs through influencing splicing, translation and decay. Recent studies suggest that m6A modification plays an important role in the progress of cardiac remodeling and cardiomyocyte contractile function. However, the exact roles of m6A in cardiovascular diseases (CVDs) have not been fully explained. In this review, we summarize the current roles of the m6A methylation in the progress of CVDs, such as cardiac remodeling, heart failure, atherosclerosis (AS), and congenital heart disease. Furthermore, we seek to explore the potential risk mechanisms of m6A in CVDs, including obesity, inflammation, adipogenesis, insulin resistance (IR), hypertension, and type 2 diabetes mellitus (T2DM), which may provide novel therapeutic targets for the treatment of CVDs.
摘要：
Atherosclerosis (AS) is widely accepted to be a multistep pathophysiological process associated with several other processes such as angiogenesis and inflammatory response. Long non-coding RNAs (lncRNAs) are non-protein coding RNAs (more than 200 nucleotides in length) and can regulate gene expression at the transcriptional and post-transcriptional levels. Recent studies suggest that lncRNA-H19 plays important roles in the regulation of angiogenesis, adipocyte differentiation, lipid metabolism, inflammatory response, cellular proliferation and apoptosis. In this review, we primarily discuss the roles of lncRNA-H19 in atherosclerosis-related pathophysiological processes and the potential mechanisms by which lncRNA-H19 regulates the development of atherosclerosis, to help provide a better understanding of the biological functions of lncRNA-H19 in atherosclerosis.
期刊：
CURRENT DRUG TARGETS,2020年21(11):1056-1067 ISSN：1389-4501
通讯作者：
Kai, Yin
作者机构：
[Zhong, Hui; Kai, Yin] Univ South China, Meng Yang Med Sch, Res Lab Translat Med, Hengyang 421001, Peoples R China.;[Kai, Yin] Guilin Med Univ, Affliated Hosp 2, Guangxi Key Lab Diabet Syst Med Guilin Med Univ, Guilin 541100, Peoples R China.;[Tang, Hui-Fang] Univ South China, Affiliated Hosp 1, Dept Cardiol, Hengyang, Hunan, Peoples R China.
通讯机构：
[Kai, Yin] G;[Kai, Yin] U;Guilin Med Univ, Affliated Hosp 2, Guangxi Key Lab Diabet Syst Med Guilin Med Univ, Guilin 541100, Peoples R China.;Univ South China, Meng Yang Med Sch, Res Lab Translat Med, Hengyang 421001, Peoples R China.
摘要：
N6-methyladenine RNA modification (m6A) is an RNA methylation modification catalyzed by methyltransferase at the 6th position nitrogen atom of adenine (A), which is the most common chemical modification of eukaryotic messenger RNA (mRNA). Recently, m6A has been found to play an important role in the dynamic regulation of RNA, which is crucial for some physiological and pathophysiological processes such as adipogenesis, cell differentiation, and the immune/inflammatory response. Metabolic diseases are a series of chronic inflammatory disorders caused by metabolic dysfunction of proteins, glucose, and lipids. Emerging studies have shown that m6A plays an important role in the process of metabolic diseases such as obesity, type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) via regulation of glucose/lipid metabolism and the immune/inflammatory response. In this review, we will summarize the role of m6A in metabolic diseases, which may provide new ideas for the prevention and treatment of metabolic diseases.
摘要：
Vascular calcification (VC), the pathological process of hydroxyapatite mineral deposition in the vascular system, is closely associated with aging, atherosclerotic plaque formation, cardiovascular disease (CVD) and diabetes mellitus (DM). Studies have shown that VC is related to cellular phenotypic changes, extracellular vesicles, disordered calcium and phosphate homeostasis, and an imbalance between inducers and inhibitors of VC. Unfortunately, there is currently no effective preventive or targeted treatment for pathologic condition. The rapid evolution of omics technology (genomics, epigenomics, transcriptomics, proteomics and metabolomics) has provided a novel approach for elucidation of pathophysiologic mechanisms in general and those associated with VC specifically. Here, we review articles published over the last twenty years and focus on the current state, challenges, limitations and future of omics in VC research and clinical practice. Highlighting potential targets based on omics technology will improve our understanding of this pathologic condition and assist in the development of potential treatment options for VC related disease.
作者机构：
[Hong Huang] Institute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang 421001, China;[Kai Yin] Center for Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, China;[Huifang Tang] Department of Cardiology, The First Affiliated Hospital of University of South China, Hengyang 421001, China
通讯机构：
[Kai Yin] C;[Huifang Tang] D;Department of Cardiology, The First Affiliated Hospital of University of South China , Hengyang 421001, China<&wdkj&>Center for Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, The Second Affiliated Hospital of Guilin Medical University , Guilin 541199, China
摘要：
The immune system plays a vital role in restoring tissue integrity and function upon injury. Wound healing is a highly dynamic process that involves early inflammatory phase, proliferative phase, and finally the maturation phase. Tissue repair begins with the formation of granulation tissue that contains macrophages to play anti-inflammatory roles. Macrophages within the granulation tissue acquire a spectrum of phase-specific phenotypes affecting fibroblast function, including myofibroblast differentiation, myofibroblast proliferation, and extracellular matrix(ECM) remodeling [1]. Nevertheless, the underlying mechanism that macrophage contributes to the myofibroblast production during tissue repair remains largely unexplored.
摘要：
As a major type of immune cells with heterogeneity and plasticity, macrophages are classically divided into inflammatory (M1) and alternative/anti-inflammatory (M2) types and play a crucial role in the progress of the inflammatory diseases. Recent studies have shown that metabolism is an important determinant of macrophage phenotype. Mitochondria, one of the most important compartments involving cell metabolism, are closely associated with the regulation of cell functions. In most types of cell, mitochondrial oxidative phosphorylation (OXPHOS) is the primary mode of cellular energy production. However, mitochondrial OXPHOS is inhibited in activated M1 macrophages, rendering them unable to be converted into M2 phenotype. Thus, mitochondrial metabolism is a crucial regulator in macrophage functions. This review summarizes the roles of mitochondria in macrophage polarization and analyzes the molecular mechanisms underlying mitochondrial metabolism and function, which may provide new approaches for the treatment of metabolic inflammatory diseases.
作者机构：
[Jiang, Zhi-Sheng; Hao, Ya-Meng; Ren, Zhong; Qu, Shun-Lin; Yin, Kai; Yuan, Hou-Qin; Wei, Dang-Heng; Liu, Lu-Shan] Univ South, Key Lab Arteriosclerosis Hunan Prov, Inst Cardiovasc Dis, Hengyang City 421001, Hunan, Peoples R China.;[Yin, Kai] Univ South China, Med Sch, Res Lab Translat Med, Hengyang 421001, Peoples R China.;[Fu, Mingui] Univ Missouri, Sch Med, Shock Trauma Res Ctr, Dept Biomed Sci, Kansas City, MO 64108 USA.;[Jiang, Zhi-Sheng] Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Jiang, Zhi-Sheng] U;Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, Hengyang 421001, Hunan, Peoples R China.
关键词：
Atherosclerosis;Endothelial cell;Endothelial to mesenchymal transition;Vascular remodeling
摘要：
Endothelial cells are the main components of the heart, blood vessels, and lymphatic vessels, which play an important role in regulating the physiological functions of the cardiovascular system. Endothelial dysfunction is involved in a variety of acute and chronic cardiovascular diseases. As a special type of epithelial-mesenchymal transition (EMT), endothelium to mesenchymal transition (EndMT) regulates the transformation of endothelial cells into mesenchymal cells accompanied by changes in the expression of various transcription factors and cytokines, which is closely related to vascular endothelial injury, vascular remodeling, myocardial fibrosis and valvar disease. Endothelial cells undergoing EndMT lose their endothelial characteristics and undergo a transition toward a more mesenchymal-like phenotype. However, the molecular mechanism of EndMT remains unclear. EndMT, as a type of endothelial dysfunction, can cause vascular remodeling which is a major determinant of atherosclerotic luminal area. Therefore, exploring the important signaling pathways in the process of EndMT may provide novel therapeutic strategies for treating atherosclerotic diseases.
