The Effect of Mineralocorticoid Receptor 3 Antagonists on Anti-Inflammatory and Anti-Fatty Acid Transport Profile in Patients with Heart Failure
Xiaoran Fu,
Cristina Almenglo,
Ángel Luis Fernandez,
José Manuel Martínez-Cereijo,
Diego Iglesias-Alvarez,
Darío Duran-Muñoz,
Tomás García-Caballero,
Jose Ramón Gonzalez-Juanatey,
Moises Rodriguez-Mañero,
Sonia Eiras
Affiliations
Xiaoran Fu
Translational Cardiology Group, Health Research Institute, 15706 Santiago de Compostela, Spain
Cristina Almenglo
Cardiology Group, Health Research Institute, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
Ángel Luis Fernandez
Heart Surgery Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
José Manuel Martínez-Cereijo
Heart Surgery Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
Diego Iglesias-Alvarez
Cardiology Group, Health Research Institute, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
Darío Duran-Muñoz
Heart Surgery Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
Tomás García-Caballero
Morphological Sciences Department, Medicine Faculty, University of Santiago de Compostela and Pathology Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
Jose Ramón Gonzalez-Juanatey
Cardiology Group, Health Research Institute, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain
Moises Rodriguez-Mañero
Translational Cardiology Group, Health Research Institute, 15706 Santiago de Compostela, Spain
Sonia Eiras
Translational Cardiology Group, Health Research Institute, 15706 Santiago de Compostela, Spain
Epicardial fat thickness is associated with cardiovascular disease. Mineralocorticoid receptor antagonist (MRA), a pharmaceutical treatment for CVD, was found to have an effect on adipose tissue. Our aim was to analyse the main epicardial fat genesis and inflammation-involved cell markers and their regulation by risk factors and MRA. We included blood and epicardial or subcutaneous fat (EAT or SAT) from 71 patients undergoing heart surgery and blood from 66 patients with heart failure. Cell types (transcripts or proteins) were analysed by real-time polymerase chain reaction or immunohistochemistry. Plasma proteins were analysed by Luminex technology or enzyme-linked immunoassay. Our results showed an upregulation of fatty acid transporter levels after aldosterone-induced genesis. The MRA intake was the main factor associated with lower levels in epicardial fat. On the contrary, MRA upregulated the levels and its secretion of the anti-inflammatory marker intelectin 1 and reduced the proliferation of epicardial fibroblasts. Our results have shown the local MRA intake effect on fatty acid transporters and anti-inflammatory marker levels and the proliferation rate on epicardial fat fibroblasts. They suggest the role of MRA on epicardial fat genesis and remodelling in patients with cardiovascular disease. Translational perspective: the knowledge of epicardial fat genesis and its modulation by drugs might be useful for improving the treatments of cardiovascular disease.
