FSCN1 is a Potential Therapeutic Target for Atherosclerosis Revealed by Single-Cell and Bulk RNA Sequencing.

Background: Atherosclerosis (AS) is the major cause of cardiovascular disease. Using integrated single-cell and bulk RNA sequencing data of atherosclerosis, we aimed to investigate the cell phenotype, intercellular communication, and potential therapeutic target in AS.

Methods: Single-cell sequencing data from aortic arch of Apoe mice in normal diet (ND) and high fat diet (HFD) groups (obtained from GSE206239) were analyzed by Seurat, singleR, ReactomeGSA, and cellchat package.

SIRT3-and FAK-mediated acetylation-phosphorylation crosstalk of NFATc1 regulates N-carboxymethyl-lysine-induced vascular calcification in diabetes mellitus.

Background And Aims: Arterial calcification is the predictor of cardiovascular risk in diabetic patients. N-carboxymethyl-lysine (CML), a toxic metabolite, is associated with accelerated vascular calcification in diabetes mellitus (DM). However, the mechanism remains elusive.

Disruption of COMMD1 accelerates diabetic atherosclerosis by promoting glycolysis.

Aims: Diabetes will lead to serious complications, of which atherosclerosis is the most dangerous. This study aimed to explore the mechanisms of diabetic atherosclerosis.

Methods: ApoE mice were fed with an high-fat diet diet and injected with streptozotocin to establish an diabetic atherosclerotic model.

[Bioinformatics analysis identifies aging/senescence-induced genes in calcified plaques].

Vascular calcification is an important pathophysiological basis of cardiovascular disease with its underlying mechanism unclear. In recent years, studies have shown that aging is one of the risk factors for vascular calcification. The purpose of this study was to investigate the microenvironmental characteristics of vascular calcification, identify aging/senescence-induced genes (ASIGs) closely related to calcified plaques, and explore the evolution trajectory of vascular calcification cell subsets.

Advances in neovascularization after diabetic ischemia.

With the high incidence of diabetes around the world, ischemic complications cause a serious influence on people's production and living. Neovascularization plays a significant role in its development. Therefore, neovascularization after diabetic ischemia has aroused attention and has become a hot spot in recent years.

Relationship Between the Triglyceride-Glucose Index and Type 2 Diabetic Macroangiopathy: A Single-Center Retrospective Analysis.

Purpose: The research explores the relationship between the triglyceride-glucose index (TyG index) and the macroangiopathy risk in single-center hospitalized type 2 diabetes mellitus (T2DM) patients and develops a risk prediction nomogram model.

Patients And Methods: A total of 858 patients with T2DM were studied retrospectively. Lasso regression was used to eliminate unimportant factors, and multivariate logistic regression analysis was used to investigate the association between the TyG index and macrovascular disease in T2DM.

Circadian rhythm disorders elevate macrophages cytokines release and promote multiple tissues/organs dysfunction in mice.

Background: Circadian rhythm disorders are severe threats to human health. The negative impact of circadian rhythm disorders on tissues/organs has not been systematically analyzed. Therefore, there is an urgent need to evaluate the damage caused by circadian rhythm disorders and explore the possible mechanisms.

Biomarkers of Blood from Patients with Atherosclerosis Based on Bioinformatics Analysis.

Atherosclerosis is a multifaceted disease characterized by the formation and accumulation of plaques that attach to arteries and cause cardiovascular disease and vascular embolism. A range of diagnostic techniques, including selective coronary angiography, stress tests, computerized tomography, and nuclear scans, assess cardiovascular disease risk and treatment targets. However, there is currently no simple blood biochemical index or biological target for the diagnosis of atherosclerosis.

Role of PI3K in the Progression and Regression of Atherosclerosis.

Phosphatidylinositol 3 kinase (PI3K) is a key molecule in the initiation of signal transduction pathways after the binding of extracellular signals to cell surface receptors. An intracellular kinase, PI3K activates multiple intracellular signaling pathways that affect cell growth, proliferation, migration, secretion, differentiation, transcription and translation. Dysregulation of PI3K activity, and as aberrant PI3K signaling, lead to a broad range of human diseases, such as cancer, immune disorders, diabetes, and cardiovascular diseases.

Role of histone deacetylase Sirt3 in the development and regression of atherosclerosis.

Atherosclerosis (AS) is the most common cause of death in cardiovascular diseases and poses severe challenges to human life and safety. Epigenetics plays a vital role in every single link of AS. Whereas, how epigenetics regulates its development and regression is still unknown.

A multi-omics view of the complex mechanism of vascular calcification.

Vascular calcification is a high incidence and high risk disease with increasing morbidity and high mortality, which is considered the consequence of smooth muscle cell transdifferentiation initiating the mechanism of accumulation of hydroxyl calcium phosphate. Vascular calcification is also thought to be strongly associated with poor outcomes in diabetes and chronic kidney disease. Numerous studies have been accomplished; however, the specific mechanism of the disease remains unclear.

Two Natural Recombination gave rise to the Coxsackievirus B3 GV that triggered outbreaks in China in 2006 - 2012.

Coxsackievirus B3 serotype GV caused the epidemic of Coxsackievirus B3 infection in China from 2006 to 2012. To study the evolution and recombination of Coxsackievirus B3 serotype GV, we performed recombination and phylogenetic analysis of 499 complete genomes of Enterovirus B available in GenBank, dated April 2019. Results indicated that most of the strains of Coxsackievirus B3 GV in P1 region were derived from a Coxsackievirus B3 GVI parent, and in P2-3 region from EchoV E25 strain, with nucleotide identities of 97.

Poliovirus serotype 2 and coxsackievirus A promote the natural recombination of poliovirus.

Poliovirus (PV) is a member of the species Enterovirus C (EV-C), which may cause irreversible paralysis and death. So, for the purpose of analyzing the evolution of PV2 to help in eradicating PVs globally, a recombination analysis was performed to verify all viral genomes of EV-C, and we found 13 putative recombination events that produced PV1, 14 recombination events that can give rise to PV2, and 9 events that can lead to PV3. By analyzing our findings, we found that PV2 was involved in 25 of 36 PV recombination events, whereas coxsackievirus A (CVA) strains were involved in 12 of 36 PV recombination events, indicating that PV2 and CVAs play major roles in the natural recombination of PV.

Echovirus plays a major role in natural recombination in the coxsackievirus B group.

Coxsakievirus (CV) B4, CVB5, and CVA9 belong to the species Enterovirus B. These viruses can cause viral encephalitis, aseptic meningitis, pancreatitis, flaccid paralysis, dilated myocarditis, and hand, foot, and mouth disease (HFMD). In order to analyze the evolution of CVB4, CVB5, and CVA9, we analyzed all of the available genome sequences of Enterovirus B (EVB) isolates and found that there were 12 putative recombination events that produced CVB4, 13 putative recombination events that produced CVB5, and 10 putative recombination events that produced CVA9.