Identification and characterization of novel ferroptosis-related genes in acute myocardial infarction.

Background: Acute myocardial infarction (AMI) is a leading cause of death and morbidity worldwide. Ferroptosis, a form of regulated cell death, plays a critical role in modulating immune functions during AMI. This study aimed to identify ferroptosis-related hub genes that could serve as potential therapeutic targets in the progression of AMI.

Associations of individual and mixture exposure to volatile organic compounds with metabolic syndrome and its components among US adults.

Background: People are exposed to various volatile organic compounds (VOCs) in their environment. Our study aims to examine the links between VOCs exposure and metabolic syndrome (MetS) and its components, as well as identify critical VOCs.

Method: In this study, we enrolled 8223 adults from the National Health and Nutrition Examination Survey (NHANES) and analyzed 15 kinds of urinary VOCs metabolites.

Association between insulin resistance and uncontrolled hypertension and arterial stiffness among US adults: a population-based study.

Background: Prior research has established the correlation between insulin resistance (IR) and hypertension. While the association between triglyceride-glucose (TyG) index, a reliable surrogate marker of IR, and uncontrolled hypertension as well as arterial stiffness among individuals with hypertension remains undisclosed.

Methods: In this study, a total of 8513 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey 1999-2018 were included.

Association between periodontitis and the prevalence and prognosis of prediabetes: a population-based study.

Background: Diagnosis and intervention of prediabetes is an emerging method for preventing diabetic progression and complications. Periodontitis has been reported to strongly correlate with the dysregulation of glucose metabolism. Nonetheless, the relationship between periodontal status and the prevalence of prediabetes as well as its prognosis remains elusive.

Association of iron status with non-alcoholic fatty liver disease and liver fibrosis in US adults: a cross-sectional study from NHANES 2017-2018.

: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder resulting in a high risk of adverse prognosis, and its presence has been considered a cause or an outcome of metabolic syndrome. But the relative factors and mechanism of NAFLD are still unclear. The aim of this study is to explore the association between iron status indicators and NAFLD as well as liver fibrosis.

A comprehensive overview of cellular senescence from 1990 to 2021: A machine learning-based bibliometric analysis.

Background: As a cellular process, senescence functions to prevent the proliferation of damaged, old and tumor-like cells, as well as participate in embryonic development, tissue repair, etc. This study aimed to analyze the themes and topics of the scientific publications related to cellular senescence in the past three decades by machine learning.

Methods: The MeSH term "cellular senescence" was used for searching publications from 1990 to 2021 on the PubMed database, while the R platform was adopted to obtain associated data.

Critical Role of Cathepsin L/V in Regulating Endothelial Cell Senescence.

The senescence of vascular endothelial cells (ECs) is characterized as a hallmark of vascular aging, which leads to the initiation, progress, and advancement of cardiovascular diseases. However, the mechanism of the ECs senescence remains elusive. In this study, thoracic aortas were separated from young (8-week-old) and aged (18-month-old) mice.

Identification and exploration of novel M2 macrophage-related biomarkers in the development of acute myocardial infarction.

Background: Acute myocardial infarction (AMI), one of the most severe and fatal cardiovascular diseases, is a major cause of morbidity and mortality worldwide. Macrophages play a critical role in ventricular remodeling after AMI. The regulatory mechanisms of the AMI progression remain unclear.

Blood and urine manganese exposure in non-alcoholic fatty liver disease and advanced liver fibrosis: an observational study.

Manganese was the key activator of biological enzymes-mediated metabolic diseases (Mets)-associated pathophysiological process. Non-alcoholic fatty liver disease (NAFLD), which was the hepatic manifestation of Mets, development remained a mystery. We aimed to explore the association between blood/urine manganese exposure and NAFLD and liver fibrosis diagnosed by vibration-controlled transient elastography (VCTE).

The association between non-alcoholic fatty liver disease (NAFLD) and advanced fibrosis with blood selenium level based on the NHANES 2017-2018.

Background & Objective: Selenium was one of the essential trace elements that played a pivotal role in human health. Although previous studies have investigated the relationship between selenium and non-alcoholic fatty liver disease (NAFLD) and fibrosis, these findings were still inconclusive. Our study was aimed to explore the association between blood selenium level and NAFLD and advanced liver fibrosis diagnosed by vibration controlled transient elastography (VCTE) in US adults.

Bioinformatics Analysis and Identification of Genes and Pathways in Ischemic Cardiomyopathy.

Purpose: Ischemic cardiomyopathy (ICM) is considered to be the most common cause of heart failure, with high prevalence and mortality. This study aimed to investigate the different expressed genes (DEGs) and pathways in the pathogenesis of ICM using bioinformatics analysis.

Methods: The control and ICM datasets GSE116250, GSE46224 and GSE5406 were collected from the gene expression omnibus (GEO) database.

Bioinformatic Analysis for Potential Biomarkers and Therapeutic Targets of T2DM-related MI.

Background: Type 2 diabetes mellitus (T2DM), a major risk factor of coronary heart disease, is associated with an approximately twofold increase in the risk of myocardial infarction (MI). We studied co-expressed genes to demonstrate relationships between DM and MI and revealed the potential biomarkers and therapeutic targets of T2DM-related MI.

Methods: DM and MI-related differentially expressed genes (DEGs) were identified by bioinformatic analysis, Gene Expression Omnibus (GEO) datasets GSE42148 and GSE61144 of MI patients, and the normal control and GSE26168 and GSE15932 of DM patients and normal controls, respectively.

A Bibliometric Analysis of 14,822 Researches on Myocardial Reperfusion Injury by Machine Learning.

Myocardial ischemia is the major cause of death worldwide, and reperfusion is the standard intervention for myocardial ischemia. However, reperfusion may cause additional damage, known as myocardial reperfusion injury, for which there is still no effective therapy. This study aims to analyze the landscape of researches concerning myocardial reperfusion injury over the past three decades by machine learning.

Peroxidasin promotes diabetic vascular endothelial dysfunction induced by advanced glycation end products via NOX2/HOCl/Akt/eNOS pathway.

Reactive oxygen species (ROS) derived from NADPH oxidases (NOX) plays an essential role in advanced glycation end products (AGEs)-induced diabetic vascular endothelial dysfunction. Peroxidasin (PXDN, VPO1) is one member of peroxidases family that catalyzes hydrogen peroxide (HO) to hypochlorous acid (HOCl). This present study aimed to elucidate the role of PXDN in promoting vascular endothelial dysfunction induced by AGEs in diabetes mellitus.

PXDN reduces autophagic flux in insulin-resistant cardiomyocytes via modulating FoxO1.

Autophagy, a well-observed intracellular lysosomal degradation process, is particularly important to the cell viability in diabetic cardiomyopathy (DCM). Peroxidasin (PXDN) is a heme-containing peroxidase that augments oxidative stress and plays an essential role in cardiovascular diseases, while whether PXDN contributes to the pathogenesis of DCM remains unknown. Here we reported the suppression of cell viability and autophagic flux, as shown by autophagosomes accumulation and increased expression level of LC3-II and p62 in cultured H9C2 and human AC16 cells that treated with 400 μM palmitate acid (PA) for 24 h.

MicroRNA-342-5p activates the Akt signaling pathway by downregulating PIK3R1 to modify the proliferation and differentiation of vascular smooth muscle cells.

Abnormal cell proliferation and invasion of vascular smooth muscle cells are among the primary causes of cardiovascular disease. Studies have shown that microRNA(miR)-342-5p participates in the development of cardiovascular diseases. The current study aimed to explore the role of miR-342-5p in the proliferation and differentiation of mouse aortic vascular smooth muscle (MOVAS) cells.

Identification of Target Genes and Transcription Factors in Mice with LMNA-Related Dilated Cardiomyopathy by Integrated Bioinformatic Analyses.

BACKGROUND Dilated cardiomyopathy (DCM), which is characterized by enlarged ventricular dimensions and systolic dysfunction, is the most common type of cardiomyopathy. Mutations in the LMNA gene are reported in approximately 10% of familial DCM cases. However, the mechanism of LMNA mutations in human DCM remains unclear.

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance.

As the standard treatments for cancer, chemotherapy and radiotherapy have been widely applied to clinical practice worldwide. However, the resistance to cancer therapies is a major challenge in clinics and scientific research, resulting in tumor recurrence and metastasis. The mechanisms of therapy resistance are complicated and result from multiple factors.

[Research progress in NADPH oxidase family in cardiovascular diseases].

Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major source of reactive oxygen species (ROS) in the cardiovascular system. The family of NOX includes seven isoforms, and expressed in different cardiovascular cell types and cell compartments, modulating multiple functions, such as cell proliferation, migration, differentiation, apoptosis, senescence, and inflammatory responses. The NOX-derived ROS are involved in many processes associated with cardiovascular diseases, such as hypertension, atherosclerosis, diabetic vascular disease, ventricular remodeling after myocardial infarction, and so on.

Vascular peroxidase 1 is a novel regulator of cardiac fibrosis after myocardial infarction.

Cardiac fibrosis is the most important mechanism contributing to cardiac remodeling after myocardial infarction (MI). VPO1 is a heme enzyme that uses hydrogen peroxide (HO) to produce hypochlorous acid (HOCl). Our previous study has demonstrated that VPO1 regulates myocardial ischemic reperfusion and renal fibrosis.

VPO1 Modulates Vascular Smooth Muscle Cell Phenotypic Switch by Activating Extracellular Signal-regulated Kinase 1/2 (ERK 1/2) in Abdominal Aortic Aneurysms.

Background Hydrogen peroxide (HO) is a critical molecular signal in the development of abdominal aortic aneurysm ( AAA ) formation. Vascular peroxidase 1 ( VPO 1) catalyzes the production of hypochlorous acid ( HOC l) from HO and significantly enhances oxidative stress. The switch from a contractile phenotype to a synthetic one in vascular smooth muscle cells ( VSMC s) is driven by reactive oxygen species and is recognized as an early and important event in AAA formation.

Vascular peroxidase 1 mediates hypoxia-induced pulmonary artery smooth muscle cell proliferation, apoptosis resistance and migration.

Aims: Reactive oxygen species (ROS) play essential roles in the pulmonary vascular remodelling associated with hypoxia-induced pulmonary hypertension (PH). Vascular peroxidase 1 (VPO1) is a newly identified haeme-containing peroxidase that accelerates oxidative stress development in the vasculature. This study aimed to determine the potential role of VPO1 in hypoxia-induced PH-related vascular remodelling.

Critical role of vascular peroxidase 1 in regulating endothelial nitric oxide synthase.

Vascular peroxidase 1 (VPO1) is a member of the peroxidase family which aggravates oxidative stress by producing hypochlorous acid (HOCl). Our previous study demonstrated that VPO1 plays a critical role in endothelial dysfunction through dimethylarginine dimethylaminohydrolase2 (DDAH2)/asymmetric Dimethylarginine (ADMA) pathway. Hereby we describe the regulatory role of VPO1 on endothelial nitric oxide synthase (eNOS) expression and activity in human umbilical vein endothelial cells (HUVECs).

Involvement of vascular peroxidase 1 in angiotensin II-induced hypertrophy of H9c2 cells.

Oxidative stress has been implicated in cardiac hypertrophy and heart failure. Vascular peroxidase 1 (VPO1), a peroxidase in the cardiovascular system, uses the hydrogen peroxide (HO) derived from co-expressed NADPH oxidases (NOX) to produce hypochlorous acid (HOCl) and catalyze peroxidative reactions. Our previous studies showed that VPO1 contributes to the vascular smooth muscle cell proliferation and endothelial dysfunction in spontaneous hypertensive rats (SHRs); however, the role of VPO1 in cardiomyocytes hypertrophy is still uninvestigated.