Publications by authors named "V Cachofeiro"

Background: Modified citrus pectin (MCP) is used as a nutritional supplement that inhibits galectin-3 activity, a central player in the cardiac damage associated with different pathological situations. In fact, we have previously observed that MCP improved cardiac function in obese infarcted rats that was associated with a reduction in cardiac fibrosis. Therefore, the aim of the present study was to further explore whether this effect could involve the modulation of gene expression of ECM components and their mediators as well as whether it could affect another two mechanisms involved in cardiac damage: mitochondrial dynamics and autophagic flux.

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Article Synopsis
  • - The study investigated the link between galectin-3 and cardiac fibrosis in patients with acute myocardial infarction (MI), finding that higher galectin-3 levels in overweight patients correlated with more severe heart damage indicators.
  • - In obese rats experiencing MI, the treatment with modified citrus pectin (MCP) and 4-phenylbutyric acid (4-PBA) improved heart health by reducing fibrosis and stress levels, and enhancing heart function over a 4-week period.
  • - The findings suggest that galectin-3 and ER stress play crucial roles in heart fibrosis related to MI in obesity, highlighting their potential as therapeutic targets for improving cardiovascular health.
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During resolution of inflammation, specialized proresolving mediators (SPMs), including resolvins, are produced to restore tissue homeostasis. We hypothesized that there might be a dysregulation of SPMs pathways in pathological vascular remodeling and that resolvin D2 (RvD2) might prevent vascular remodeling and contractile and endothelial dysfunction in a model of obesity and hypertension. In aortic samples of patients with or without abdominal aortic aneurysms (AAA), we evaluated gene expression of enzymes involved in SPMs synthesis (ALOXs), SPMs receptors and pro-inflammatory genes.

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Article Synopsis
  • Cardiovascular disease (CVD) is the leading cause of death globally, with myocardial infarction (MI) being the most common form, resulting from insufficient oxygen supply to the heart muscle.
  • MI leads to changes in heart structure, increasing the risk of heart failure and death, making it essential to create animal models that imitate human heart disease for research and therapy development.
  • The text outlines a method for inducing MI in rats with a low mortality rate (<15%) and describes imaging techniques, like echocardiography and magnetic resonance, to assess heart structure and function, aiding both acute and chronic research studies.
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Background: Over the past years, information about the crosstalk between the epicardial adipose tissue (EAT) and the cardiovascular system has emerged. Notably, in the context of acute myocardial infarction (AMI), EAT might have a potential role in the pathophysiology of ventricular structural changes and function, and the clinical evolution of patients. This study aims to assess the impact of EAT on morpho-functional changes in the left ventricle (LV) and the outcome of patients after an AMI.

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