Critical gene signature and immunological characterization in peripheral vascular atherosclerosis: novel insights from mendelian randomization and transcriptomics.

Introduction: Peripheral vascular atherosclerosis (PVA) is a chronic inflammatory disease characterized by lipid accumulation in blood vessel walls, leading to vessel narrowing and inadequate blood supply. However, the molecular mechanisms underlying PVA remain poorly understood. In this study, we employed a combination of Mendelian randomization (MR) analysis and integrated transcriptomics to identify the critical gene signature associated with PVA.

Nuciferine reduces vascular leakage and improves cardiac function in acute myocardial infarction by regulating the PI3K/AKT pathway.

The destruction of the microvascular structure and function can seriously affect the survival and prognosis of patients with acute myocardial infarction (AMI). Nuciferine has a potentially beneficial effect in the treatment of cardiovascular disease, albeit its role in microvascular structure and function during AMI remains unclear. This study aimed to investigate the protective effect and the related mechanisms of nuciferine in microvascular injury during AMI.

Multi-scale bioimpedance flexible sensing with causal hierarchical machine learning for fish vitality evaluation under adversity stress.

It is expected that waterless low-temperature stressful environments will induce stress responses in fish and affect their vitality. In this study, we developed a laser-activated, stretchable, highly conductive liquid metal (LM) based flexible sensor system for fish multi-scale bioimpedance detection. It has excellent conformability, electrical conductivity, bending and cyclic tensile stability.

Prediction of acute kidney injury incidence following acute type A aortic dissection surgery with novel biomarkers: a prospective observational study.

Background: Acute kidney injury (AKI) is a prevalent complication following acute type A aortic dissection (ATAAD) surgery and is closely associated with unfavorable prognostic outcomes. Hence, the development of a robust and efficient diagnostic approach to identify high-risk patients is of paramount importance.

Methods: We conducted a prospective study involving 328 patients who underwent ATAAD surgery at our institution, comprising three distinct cohorts.

A 2-decade bibliometric analysis of epigenetics of cardiovascular disease: from past to present.

Background: Cardiovascular disease (CVD) remains a major health killer worldwide, and the role of epigenetic regulation in CVD has been widely studied in recent decades. Herein, we perform a bibliometric study to decipher how research topics in this field have evolved during the past 2 decades.

Results: Publications on epigenetics in CVD produced during the period 2000-2022 were retrieved from the Web of Science Core Collection (WoSCC).

NAT10 Is Involved in Cardiac Remodeling Through ac4C-Mediated Transcriptomic Regulation.

Background: Heart failure, characterized by cardiac remodeling, is associated with abnormal epigenetic processes and aberrant gene expression. Here, we aimed to elucidate the effects and mechanisms of NAT10 (N-acetyltransferase 10)-mediated N4-acetylcytidine (ac4C) acetylation during cardiac remodeling.

Methods: NAT10 and ac4C expression were detected in both human and mouse subjects with cardiac remodeling through multiple assays.

Endothelial HDAC1-ZEB2-NuRD Complex Drives Aortic Aneurysm and Dissection Through Regulation of Protein S-Sulfhydration.

Background: Aortic aneurysm and aortic dissection (AAD) are life-threatening vascular diseases, with endothelium being the primary target for AAD treatment. Protein S-sulfhydration is a newly discovered posttranslational modification whose role in AAD has not yet been defined. This study aims to investigate whether protein S-sulfhydration in the endothelium regulates AAD and its underlying mechanism.

Protein Persulfidation: Recent Progress and Future Directions.

Hydrogen sulfide (HS) is considered to be a gasotransmitter along with carbon monoxide (CO) and nitric oxide (NO), and is known as a key regulator of physiological and pathological activities. S-sulfhydration (also known as persulfidation), a mechanism involving the formation of protein persulfides by modification of cysteine residues, is proposed here to explain the multiple biological functions of HS. Investigating the properties of protein persulfides can provide a foundation for further understanding of the potential functions of HS.

Automatic algorithm for the characterization of sweat ducts in a three-dimensional fingerprint.

In this study, an automatic algorithm has been presented based on a convolutional neural network (CNN) employing U-net. An ellipsoid and an ellipse were applied for approximation of a three-dimensional sweat duct and en face sweat pore at the different depths, respectively. The results demonstrated that the length and the diameter of the ellipsoid can be used to quantitatively describe the sweat ducts, which has a potential for estimating the frequency of resonance in millimeter (mm) wave and terahertz (THz) wave.

S-nitrosylation-mediated coupling of G-protein alpha-2 with CXCR5 induces Hippo/YAP-dependent diabetes-accelerated atherosclerosis.

Atherosclerosis-associated cardiovascular disease is one of the main causes of death and disability among patients with diabetes mellitus. However, little is known about the impact of S-nitrosylation in diabetes-accelerated atherosclerosis. Here, we show increased levels of S-nitrosylation of guanine nucleotide-binding protein G(i) subunit alpha-2 (SNO-GNAI2) at Cysteine 66 in coronary artery samples from diabetic patients with atherosclerosis, consistently with results from mice.

Dioscin elevates lncRNA MANTIS in therapeutic angiogenesis for heart diseases.

Dioscin has been widely used in clinics for coronary artery disease (CAD) treatment for years in China. However, the underlying mechanism for Dioscin-mediated cardioprotective effect has not been elucidated. Here, we showed that Dioscin significantly rescues the cardiac function in mouse model of myocardial infarction (MI), accompanied by the reduction of cardiac fibrosis and apoptosis, resulting from elevated angiogenesis.

eNOS S-nitrosylation mediated OxLDL-induced endothelial dysfunction via increasing the interaction of eNOS with β‑catenin.

Protein S-nitrosylation plays an important role in the progression of cardiovascular diseases. eNOS can be S-nitrosylated in endothelial cells, and this modification reversibly attenuates enzyme activity. Under physiological conditions, eNOS directly interacts with β‑catenin.