Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage

Author:

Schiano Concetta12ORCID,Balbi Carolina2ORCID,de Nigris Filomena3ORCID,Napoli Claudio14

Affiliation:

1. Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania Luigi Vanvitelli, 80138 Naples, Italy

2. Laboratory of Cellular and Molecular Cardiology, Cardiocentro Ticino Institute, 6807 Taverne-Torricella, Switzerland

3. Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Naples, Italy

4. Clinical Department of Internal Medicine and Specialistic Units, Division of Clinical Immunology and Immunohematology, Transfusion Medicine and Transplant Immunology (SIMT), Azienda Universitaria Policlinico (AOU), 80138 Naples, Italy

Abstract

Both progression from the early pathogenic events to clinically manifest cardiovascular diseases (CVD) and cancer impact the integrity of the vascular system. Pathological vascular modifications are affected by interplay between endothelial cells and their microenvironment. Soluble factors, extracellular matrix molecules and extracellular vesicles (EVs) are emerging determinants of this network that trigger specific signals in target cells. EVs have gained attention as package of molecules with epigenetic reversible activity causing functional vascular changes, but their mechanisms are not well understood. Valuable insights have been provided by recent clinical studies, including the investigation of EVs as potential biomarkers of these diseases. In this paper, we review the role and the mechanism of exosomal epigenetic molecules during the vascular remodeling in coronary heart disease as well as in cancer-associated neoangiogenesis.

Funder

Italian Ministry of University and Research

Italian Ministry of Health

Swiss Heart Foundation

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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