Publications by authors named "M F Crescente"
Article Synopsis
- Heart failure is a big health issue, and doctors are exploring new treatments like vagus nerve stimulation (VNS), which uses devices to help the heart.
- A study on rats looked at how VNS affects the heart's genes and found 294 genes that changed when the vagus nerve was stimulated with light.
- The results suggest that VNS can help the heart by influencing important processes like inflammation, protein production, and heart growth, showing that keeping the vagus nerve active might be good for heart health.
Background: Extracellular traps formed by neutrophils (NETs) and eosinophils (EETs) have been described in coronary thrombi, contributing to thrombus stability. A key mechanism during NET formation is histone modification by the enzyme PAD4. Citrullinated histones, the product of PAD4 activity, are often attributed to neutrophils.
View Article and Find Full Text PDFHeart failure is a major clinical problem, with treatments involving medication, devices, and emerging neuromodulation therapies such as vagus nerve stimulation (VNS). Considering the ongoing interest in using VNS to treat cardiovascular disease, it is important to understand the genetic and molecular changes developing in the heart in response to this form of autonomic neuromodulation. This experimental animal (rat) study investigated the immediate transcriptional response of the ventricular myocardium to selective stimulation of vagal efferent activity using an optogenetic approach.
View Article and Find Full Text PDFIntroduction: Through the production of prostacyclin, cyclooxygenase (COX)-2 protects the cardiorenal system. Asymmetric dimethylarginine (ADMA), is a biomarker of cardiovascular and renal disease. Here we determined the relationship between COX-2/prostacyclin, ADMA, and renal function in mouse and human models.
View Article and Find Full Text PDFArticle Synopsis
- Thrombosis in the lung microvasculature is a common feature of severe COVID-19, likely caused by the activation of specific proteins in the lungs, distinct from other types of respiratory distress.
- Researchers identified that the Spike protein from SARS-CoV-2 activates the TMEM16F channel, which is crucial for promoting platelet activity and thrombus formation.
- Drugs Niclosamide and Clofazimine were found to effectively inhibit this Spike-induced platelet activation, suggesting a potential therapeutic approach to treat COVID-19-related lung thrombosis by disrupting this pathogenic mechanism.