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Updated: Aug 1, 2025

Evaluation of the Storage Stability of Extracellular Vesicles
Published on: May 22, 2019
Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage
Concetta Schiano1,2, Carolina Balbi2, Filomena de Nigris3
1Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania Luigi Vanvitelli, 80138 Naples, Italy.
Extracellular vesicles (EVs) mediate vascular remodeling in cardiovascular diseases and cancer. This review explores how exosomal epigenetic molecules drive vascular changes and their potential as disease biomarkers.
Area of Science:
- Vascular biology and epigenetics
- Cardiovascular diseases and oncology
- Extracellular vesicle biology
Background:
- Cardiovascular diseases (CVD) and cancer compromise vascular integrity.
- Endothelial cells and their microenvironment interactions are key to vascular remodeling.
- Extracellular vesicles (EVs) are emerging as critical mediators of cellular communication and disease progression.
Purpose of the Study:
- To review the role of exosomal epigenetic molecules in vascular remodeling.
- To elucidate the mechanisms by which EVs influence cardiovascular disease and cancer-associated neoangiogenesis.
- To highlight the potential of EVs as biomarkers for these pathologies.
Main Methods:
- Literature review focusing on exosomal epigenetic mechanisms.
- Analysis of recent clinical studies on EVs in CVD and cancer.
- Synthesis of current understanding of EV-mediated vascular changes.
Main Results:
- EVs carry epigenetic factors that induce functional vascular changes.
- Exosomal epigenetic molecules play a significant role in coronary heart disease vascular remodeling.
- EVs are implicated in cancer-associated neoangiogenesis through epigenetic modulation.
Conclusions:
- Exosomal epigenetic molecules are crucial regulators of vascular remodeling in CVD and cancer.
- Understanding EV mechanisms offers insights into disease pathogenesis.
- EVs show promise as diagnostic and prognostic biomarkers.
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