Extracellular vesicles isolated from patients with heart failure retain proinflammatory features
Selected Abstract – Spring Meeting 2026
Copyright (c) 2026 Isabella Fichtner , Chiara Macchi, Fran Tafuri, Alessandra S. Rizzuto, Alberto Corsini, Ilaria Giusti, Giovanni Esposito, Cinzia Perrino, Stefano Carugo, Marco Vincenzi, Massimiliano Ruscica
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
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Published: April 30, 2026
Abstract
Aim Heart failure (HF) is a clinical syndrome involving structural and/or functional cardiac abnormalities, classified as reduced (HFrEF) or preserved (HFpEF) based on the ejection fraction percentage of the left ventricle. As extracellular vesicles (EVs) reflect onset and severity of cardiac diseases, they attract interest as potential liquid biopsies. Aim of the present project was to characterize EVs in HF patients, investigating their potential as biomarkers and tools to discriminate between HFrEF and HFpEF clinical phenotypes.
Methods The study included 39 HF patients (13 HFpEF and 26 HFrEF) and 28 volunteers (CTR). EVs were isolated from plasma by size-exclusion chromatography and ultracentrifugation, then characterized using nanoparticles tracking analysis, transmission electron microscopy (TEM), Western blot (WB) and flow cytometry (FACS). Functional assays using patient-derived EVs were performed on cellular models of monocyte (THP-1) and cardiomyocyte (H9C2).
Results Diagnosis of HF relied on echocardiographic (e.g. E/e' ratio) and biochemical parameters (e.g. NT-proBNP). Isolation of EV was confirmed by FACS and WB analyses (e.g. the presence of CD63, CD9, CD81, Alix and β1 integrin), while integrity by TEM. EV size was increased in HF (nm: 202 vs 181). Among different subpopulations of EVs, those from monocytes (CD14+), macrophages (CD206+), neutrophils (CD66b+), endothelial cells (CD202b+), activated endothelial cells (CD62E+), cardiomyocytes (CD172a+), platelets (CD41a+), were significantly reduced in HF. Conversely, EVs released by T helper lymphocytes (CD4+) were significantly increased in HF patients when compared to controls. Treatment of THP-1 and H9C2 cells with EVs derived from HF patients led to an increased expression of proinflammatory cytokines (i.e. IL-1, IL-1, IL-6), when compared to cells treated with EVs isolated from CTR subjects. This change was mostly driven by EVs derived from HFpEF patients.
Conclusions EVs derived from HF patients exhibit a distinct profile that reflects the hemodynamic characteristics of the condition and possess proinflammatory properties.
