Identification and functional characterization of differentially expressed circRNAs in high glucose treated endothelial cells: Construction of circRNA-miRNA-mRNA network.

Background: Endothelial dysfunction is a complication of diabetes mellitus (DM), characterized by impaired endothelial function in both microvessels and macrovessels, closely linked to atherosclerosis (AS). Endothelial dysfunction, characterized by impaired endothelial cell (EC) function, is a pivotal factor in AS and DM. Circular RNAs (circRNAs) are endogenous non-coding RNAs that can act as competing endogenous RNAs (ceRNAs) and regulate gene expression.

Corrigendum: Single-cell RNA sequencing of peripheral blood mononuclear cells from acute myocardial infarction.

[This corrects the article DOI: 10.3389/fimmu.2022.

Impact of Radial Wall Strain on Serial Changes in Vascular Physiology in Patients with Intermediate Coronary Stenosis.

Background: Coronary biomechanical stress contributes to the plaque rupture and subsequent events. This study aimed to investigate the impact of plaque biomechanical stability on the physiological progression of intermediate lesions, as assessed by the radial wall strain (RWS) derived from coronary angiography.

Methods: Patients with at least one medically treated intermediate lesion at baseline who underwent follow-up coronary angiography over 6 months were included.

KLF4 inhibited the senescence-associated secretory phenotype in ox-LDL-treated endothelial cells via PDGFRA/NAMPT/mitochondrial ROS.

Background: Inflammation is one of the significant consequences of ox-LDL-induced endothelial cell (EC) dysfunction. The senescence-associated secretory phenotype (SASP) is a critical source of inflammation factors. However, the molecular mechanism by which the SASP is regulated in ECs under ox-LDL conditions remains unknown.

The relationship between glycemic risk and longitudinal changes in total physiological atherosclerotic burden in patients with coronary artery disease.

Background: The effects of glycemic status on coronary physiology have not been well evaluated. This study aimed to investigate changes in coronary physiology by using angiographic quantitative flow ratio (QFR), and their relationships with diabetes mellitus (DM) and glycemic control status.

Methods: This retrospective cohort study included 530 patients who underwent serial coronary angiography (CAG) measurements between January 2016 and December 2021 at Tongji Hospital of Tongji University.

Prognostic Implications of Changes in Total Physiological Atherosclerotic Burden in Patients With Coronary Artery Disease-A Serial QFR Study.

The association between coronary physiological progression and clinical outcomes has not been investigated. A total of 421 patients who underwent serial coronary angiography at least 6 months apart were included. Total physiological atherosclerotic burden was characterized by sum of quantitative flow ratio in 3 epicardial vessels (3V-QFR).

MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1.

Myocardial infarction (MI) is a leading cause of mortality. To better understand its molecular and cellular mechanisms, we used bioinformatic tools and molecular experiments to explore the pathogenesis and prognostic markers. Differential gene expression analysis was conducted using GSE60993 and GSE66360 datasets.

Screening of Potential Circulating Diagnostic Biomarkers and Molecular Mechanisms of Systemic Lupus Erythematosus-Related Myocardial Infarction by Integrative Analysis.

Background: The risk of acute myocardial infarction (AMI) is elevated in patients with systemic lupus erythematosus (SLE), and it is of great clinical value to identify potential molecular mechanisms and diagnostic markers of AMI associated with SLE by analyzing public database data and transcriptome sequencing data.

Methods: AMI and SLE-related sequencing datasets GSE62646, GSE60993, GSE50772 and GSE81622 were downloaded from the Gene Expression Omnibus (GEO) database and divided into prediction and validation cohorts. To identify the key genes associated with AMI related to SLE, WGCNA and DEGs analysis were performed for the prediction and validation cohorts, respectively.

New Concepts on the Pathophysiology of Acute Coronary Syndrome.

Acute coronary syndrome (ACS) is the most severe form of ischemic heart disease. Although it is caused by atherosclerotic plaque thrombosis or nonatherosclerotic causes, its pathophysiological mechanism of ACS is not fully understood, and its concept is constantly updated and developed. At present, the main pathophysiological mechanisms include plaque rupture, plaque erosion, calcified nodules (CN) and non-atherosclerotic causes such as coronary vasospasm and myocardial bridging (MB).

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis.

Homocysteine (Hcy) is an intermediate amino acid formed during the conversion from methionine to cysteine. When the fasting plasma Hcy level is higher than 15 μmol/L, it is considered as hyperhomocysteinemia (HHcy). The vascular endothelium is an important barrier to vascular homeostasis, and its impairment is the initiation of atherosclerosis (AS).

Angiographic quantitative flow ratio in acute coronary syndrome: beyond a tool to define ischemia-causing stenosis-a literature review.

Background And Objective: Numerous studies have demonstrated the safety and effectiveness of physiology-guided coronary revascularization in chronic coronary syndrome, resulting in a high level of guideline recommendation for these patients. However, the application of coronary physiology in acute coronary syndrome (ACS), especially in the acute phase of myocardial infarction, remains challenging. Over the last decade, the number of novel physiological indices derived from the computation of angiography have been developed as alternatives to pressure wire-based fractional flow reserve.

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction.

Background: Acute myocardial infarction (AMI) can occur in patients with atherosclerotic disease, with or without plaque rupture. Previous studies have indicated a set of immune responses to plaque rupture. However, the specific circulating immune cell subsets that mediate inflammatory plaque rupture remain elusive.

miR-126-5p enhances radiosensitivity of lung adenocarcinoma cells by inhibiting EZH2 via the KLF2/BIRC axis.

Radiotherapy is a common method for the treatment of lung adenocarcinoma, but it often fails due to the relative non-susceptibility of lung adenocarcinoma cells to radiation. We aimed to discuss the related mechanisms by which miR-126-5p might mediate radiosensitivity of lung adenocarcinoma cells. The binding affinity between miR-126-5p and EZH2 and between KLF2 and BIRC5 was identified using multiple assays.

FeO magnetic nanoparticle-enhanced radiotherapy for lung adenocarcinoma via delivery of siBIRC5 and AS-ODN.

Background: Radiotherapy is the mainstay treatment for lung adenocarcinoma, yet remains highly susceptible to resistance. FeO magnetic nanoparticles (MNPs) possess the ability to induce biological therapeutic effects. Herein, the current study set out to explore the effects of FeO MNPs on radiosensitivity of lung adenocarcinoma cells.

Clinical implication of quantitative flow ratio to predict clinical events after drug-coated balloon angioplasty in patients with in-stent restenosis.

Background: The association between the quantitative flow ratio (QFR) and adverse events after drug-coated balloon (DCB) angioplasty for in-stent restenosis (ISR) lesions has not been investigated.

Hypothesis: Post-procedural QFR is related to adverse events in patients undergoing DCB angioplasty for ISR lesions.

Methods: This retrospective study included data from patients undergoing DCB angioplasty for drug-eluting stent (DES) ISR between January 2016 and February 2019.

Association of stress hyperglycemia ratio with intracoronary thrombus burden in diabetic patients with ST-segment elevation myocardial infarction.

Background: Large intracoronary thrombus burden is not rare during primary percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). Stress hyperglycemia is independently associated with poor prognosis. However, the underlying relationship between stress hyperglycemia and thrombus burden remains unknown.

Clinical implication of QFR in patients with ST-segment elevation myocardial infarction after drug-eluting stent implantation.

The feasibility and prognostic value of quantitative flow ratio (QFR) after percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) patients have not been assessed. The aim of this study was to investigate the prognostic utility of post-PCI QFR to predict outcomes in STEMI and determine the influence of functional results, in both culprit and nonculprit lesions, after PCI. Patients undergoing PCI of culprit lesions and receiving staged procedures of nonculprit lesions after 7 days were enrolled from 2 centers and underwent post-PCI QFR.

Quantitative flow ratio-guided residual functional SYNTAX score for risk assessment in patients with ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention.

Background: Functional incomplete revascularisation (IR) is associated with a higher risk of major adverse cardiac events (MACE) during long-term follow-up in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI).

Aims: This study aimed to investigate the prognostic ability of quantitative flow ratio (QFR)-guided residual functional SYNTAX score (Q-rFSS) and functional IR in STEMI patients undergoing PCI.

Methods: In total, 354 consecutive STEMI patients who successfully underwent PCI were included.