Extracellular Vesicles as Mediators of Pathophysiology and Disease Progression in Cardiovascular Diseases
TL;DR
It is confirmed that EVs carry disease-specific molecular cargo, particularly microRNAs, long non-coding RNAs, proteins, and other bioactive molecules, contributing to inflammation, oxidative stress, fibrosis, endothelial dysfunction, and cardiac remodeling, while also serving as promising diagnostic and prognostic biomarkers.
Abstract
The rising prevalence of cardiovascular diseases (CVDs) worldwide imposes a substantial economic burden on healthcare systems. Despite major advances in evidence-based therapies and modern healthcare, the demand for novel, time- and cost-effective treatment options continues to grow. Extracellular vesicles (EVs), including apoptotic bodies, microvesicles, and exosomes, are released by numerous cell types and mediate intercellular communication in both physiological and pathological contexts. To date, researchers have amassed compelling evidence for the functional roles of EVs in the development and progression of myocardial disease, supporting their exploration for clinical applications. In this review, we examine the multifunctional roles of EVs from diverse cellular origins in prominent CVD manifestations, highlighting publications of the last eight years and their key findings. They confirm that EVs carry disease-specific molecular cargo, particularly microRNAs, long non-coding RNAs, proteins, and other bioactive molecules, contributing to inflammation, oxidative stress, fibrosis, endothelial dysfunction, and cardiac remodeling, while also serving as promising diagnostic and prognostic biomarkers. Furthermore, emerging preclinical evidence demonstrates the therapeutic potential of engineered or tissue-derived EVs for promoting cardiac repair and limiting adverse cardiac remodeling.