Galectin-3 and soluble RAGE as new biomarkers of post-infarction cardiac remodeling.

Post-infarction remodeling is a clinical problem with no curative treatment. Our objective was to search for new biomarkers of cardiac remodeling that have clinical value after ST-segment elevation myocardial infarction (STEMI). This pilot study enrolled 67 consecutive patients with de novo STEMI who underwent revascularization by primary angioplasty.

The different roles for the advanced glycation end products axis in heart failure and acute coronary syndrome settings.

Aims: This work aimed to compare the behavior of the advanced glycation end products (AGEs) and their soluble receptor (sRAGE) in two cohorts of patients: those with heart failure (HF) and acute coronary syndrome (ACS).

Methods And Results: A unicentric observational clinical study was performed in 102 patients with ACS and 102 patients with chronic HF matched by age and gender. At inclusion, fluorescent AGEs were measured by quantitative fluorescence spectroscopy of plasma, and total sRAGE and endogenous secretory RAGE (esRAGE) levels were determined by enzyme-linked immunosorbent assay kits.

Obesity-Related Genetic Determinants of Heart Failure Prognosis.

Purpose: Recent advances in genomics offer a smart option for predicting future risk of disease and prognosis. The objective of this study was to examine the prognostic value in heart failure (HF) patients, of a series of single nucleotide polymorphisms (SNPs).

Methods: A selection of 192 SNPs found to be related with obesity, body mass index, circulating lipids or cardiovascular diseases were genotyped in 191 patients with HF.

Inflammatory effects of in vivo glycated albumin from cardiovascular patients.

Objectives: Characterization of the type of glycation found in circulating proteins from cardiovascular patients in comparison with healthy control subjects and to explore the pathophysiological molecular effects of these glycomodified proteins on human umbilical vein endothelial cells (HUVEC) in culture.

Methods: Human serum albumin pools from 10 subjects each, of patients with heart failure (HF) presenting high or low glycation levels, and from healthy subjects were isolated and purified. The glycation levels of these pools were characterized by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and compared between them.

Advanced glycation end-products disrupt human endothelial cells redox homeostasis: new insights into reactive oxygen species production.

Advanced glycation end-products (AGEs) trigger multiple metabolic disorders in the vessel wall that may in turn lead to endothelial dysfunction. The molecular mechanisms by which AGEs generate these effects are not completely understood. Oxidative stress plays a key role in the development of deleterious effects that occur in endothelium during diabetes.

Glycation of human serum albumin impairs binding to the glucagon-like peptide-1 analogue liraglutide.

The long-acting glucagon-like peptide-1 analogue liraglutide has proven efficiency in the management of type 2 diabetes and also has beneficial effects on cardiovascular diseases. Liraglutide's protracted action highly depends on its capacity to bind to albumin via its palmitic acid part. However, in diabetes, albumin can undergo glycation, resulting in impaired drug binding.

Protective, repairing and fibrinolytic effects of rivaroxaban on vascular endothelium.

Aims: Rivaroxaban, a direct inhibitor of activated factor X (FXa), is the only new oral anticoagulant approved for secondary prevention after acute coronary syndrome. Our objective was to identify the possible molecular mechanisms of rivaroxaban that contribute to endothelial function.

Methods: Cell viability and growth of human umbilical vein endothelial cells (HUVEC) were registered.

Evolution and bad prognostic value of advanced glycation end products after acute heart failure: relation with body composition.

Aim: The role of advanced glycation end products (AGEs) and their soluble receptor (sRAGE) on the progression and prognosis of acute heart failure (HF) was analysed in relation with metabolic parameters as body composition and nutritional status.

Methods: A hundred and fifty consecutive patients were included in a prospective clinical study during hospitalization by acute HF. Detailed medical history, physical examination, electrocardiogram, echocardiogram and vein peripheral blood were taken for all patients.

Diabetes-induced hepatic oxidative stress: a new pathogenic role for glycated albumin.

Increased oxidative stress and advanced glycation end-product (AGE) formation are major contributors to the development of type 2 diabetes. Here plasma proteins e.g.

Endothelial progenitor cells mobilisation after percutaneous coronary intervention: a pilot study.

Background: The mobilisation process of endothelial progenitor cells (EPC) after stent implantation by percutaneous coronary intervention (PCI) is unclear because the circulating EPC levels are influenced by several pathophysiological factors. The objective was to analyse the kinetics of EPC concentration following elective PCI in patients with stable angina, and its relation with other biomarkers or parameters of cardiovascular function.

Methods: Pilot study in stable angina patients (n = 30) for elective PCI and implantation of bare-metal stent (BMS), drug-eluting stent (DES) or EPC-capturing stent (ECS).

Change of concept about the regulation of angiotensin II-induced monocyte chemoattractant protein-1 production in human endothelial cells.

Aims: Some intriguing clinical observations about the anti-inflammatory effects of angiotensin type 1 (AT1) receptor blockers and angiotensin converting enzyme inhibitors in cardiovascular patients brought us to study the signalling pathways which lead to angiotensin II (ANG)-induced monocyte chemoattractant protein-1 (MCP-1) production in human endothelial cells.

Methods: MCP-1 production in human umbilical vein endothelial cells (HUVECs) under treatments with ANG, AT1 and angiotensin type 2 (AT2) receptor blockers and pravastatin was measured by ELISA. The expression of AT1 and AT2 receptors and NADPH oxidase catalytic subunits (NOX 1-5) was analysed at mRNA and protein levels.

Sea cucumbers with an anti-inflammatory effect on endothelial cells and subcutaneous but not on epicardial adipose tissue.

Objective: epicardial adipose tissue (EAT) from patients with coronary artery disease (CAD) contains higher levels of inflammatory proteins and lower adiponectin levels than subcutaneous adipose tissue (SAT), enhancing the progression of atherosclerosis. Since products from sea cucumber have anti-inflammatory properties, we investigated its effect on EAT, SAT and endothelial cells.

Methods: stromal cells or explants from EAT and SAT were obtained from patients with cardiovascular disease.

Key structural and functional differences between early and advanced glycation products.

Most of the studies on advanced glycation end products (AGE) have been carried out with uncharacterized mixtures of AGE, so the observed effects cannot be linked to defined structures. Therefore, we analysed the structural differences between glycated human serum albumin (gHSA), a low glycated protein, and AGE-human serum albumin (AGE-HSA), a high glycated protein, and we compared their effects on endothelial functionality. Specifically, we characterized glycation and composition on both early and advanced stage glycation products of gHSA and AGE-HSA by using the MALDI-TOF-mass spectrometry assay.

Glucose and Inflammatory Cells Decrease Adiponectin in Epicardial Adipose Tissue Cells: Paracrine Consequences on Vascular Endothelium.

Epicardial adipose tissue (EAT) is a source of energy for heart that expresses the insulin-sensitizer, anti-inflammatory and anti-atherogenic protein, adiponectin. But, in coronary artery disease, adiponectin production declines. Our objective was to determine its regulation by glucose and inflammation in stromal cells from EAT and subcutaneous adipose tissue (SAT) and its paracrine effect on endothelial cells.

Glycated human serum albumin induces NF-κB activation and endothelial nitric oxide synthase uncoupling in human umbilical vein endothelial cells.

Aims: Non-enzymatic glycated proteins could mediate diabetes vascular complications, but the molecular mechanisms are unknown. Our objective was to find new targets involved in the glycated human serum albumin (gHSA)-enhanced extracellular reactive oxygen species (ROS) production in human endothelial cells.

Methods & Results: Some nuclear factors and phosphorylation cascades were analysed.

The downregulation of ΔNp63 in p53-deficient mouse epidermal tumors favors metastatic behavior.

The TP63 gene codes for two major isoform types, TAp63 and ΔNp63, with probable opposite roles in tumorigenesis. The ΔNp63α protein is frequently amplified and overexpressed in different epithelial tumors. Accordingly, it has been considered a potential oncogene.

Advanced glycation end-products as long-term predictors of death and reinfarction after an acute coronary syndrome.

Aim: We evaluated the prognostic value of plasmatic fluorescent advanced glycation end-products (AGE) to predict long-term death and reinfarction in patients with acute coronary syndrome (ACS).

Materials & Methods: A unicenter registry comprising a prospective cohort of 210 ACS patients (47.4% ST-segment elevation myocardial infarction) followed up during 3.

Fluorescent advanced glycation end products and their soluble receptor: the birth of new plasmatic biomarkers for risk stratification of acute coronary syndrome.

Objective: Advanced glycation end products (AGEs) have pathophysiological implications in cardiovascular diseases. The aim of our study was to evaluate the prognostic value of fluorescent AGEs and its soluble receptor (sRAGE) in the context of acute coronary syndrome (ACS), both in-hospital phase and follow-up period.

Methods: A prospective clinical study was performed in patients with debut's ACS.

Current status of NADPH oxidase research in cardiovascular pharmacology.

The implications of reactive oxygen species in cardiovascular disease have been known for some decades. Rationally, therapeutic antioxidant strategies combating oxidative stress have been developed, but the results of clinical trials have not been as good as expected. Therefore, to move forward in the design of new therapeutic strategies for cardiovascular disease based on prevention of production of reactive oxygen species, steps must be taken on two fronts, ie, comprehension of reduction-oxidation signaling pathways and the pathophysiologic roles of reactive oxygen species, and development of new, less toxic, and more selective nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors, to clarify both the role of each NADPH oxidase isoform and their utility in clinical practice.

Statins modulate feedback regulation mechanisms between advanced glycation end-products and C-reactive protein: evidence in patients with acute myocardial infarction.

Objective: High sensitivity C-reactive protein (hsCRP) and advanced glycation end-products (AGEs) have been proposed as mediators in inflammation and atherosclerosis. Therefore, we studied the relation between AGE and hsCRP in patients with acute myocardial infarction (AMI).

Methods: Patients with AMI diagnosis and satisfying our inclusion criteria were included during 2009-2011 in an unicentre registry of AMI patients for a cross-sectional study.

High-sensitivity C-reactive protein predicts adverse outcomes after non-ST-segment elevation acute coronary syndrome regardless of GRACE risk score, but not after ST-segment elevation myocardial infarction.

Introduction: Atherosclerosis is an active process and the inflammatory component appears to be particularly correlated with the development of acute coronary syndromes (ACS). C-reactive protein (CRP) is an acute phase protein that appears in the circulation in response to inflammatory cytokines. The present study investigated the association between high-sensitivity C-reactive protein (hsCRP) on admission and follow-up prognosis after an ACS.

Predictive value of advanced glycation end products for the development of post-infarction heart failure: a preliminary report.

Background: Since post-infarction heart failure (HF) determines a great morbidity and mortality, and given the physiopathology implications of advanced glycation end products (AGE) in the genesis of myocardial dysfunction, it was intended to analyze the prognostic value of these molecules in order to predict post-infarction HF development.

Methods: A prospective clinical study in patients after first acute coronary syndrome was conducted. The follow-up period was consisted in 1 year.