4.7 Review

Role of Extracellular Vesicles as Potential Diagnostic and/or Therapeutic Biomarkers in Chronic Cardiovascular Diseases

Journal

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2022.813885

Keywords

extracelular vesicles; vascular smooth muscle cells; calcification; aneurysm; peripheral arterial disease

Funding

  1. Spanish Ministry of Economy and Competitiveness [PID2019-106814RB-I00]
  2. Comunidad Autonoma de Madrid (Complemento II-CM) [S2017/BMD-3673]
  3. Instituto de Salud Carlos III (ISCiii-FEDER) [IPT17/0019, PI18/01195, PI19/00065 PI19/00128, RD21/0006/0008]
  4. European Regional Development Fund A way to make Europe
  5. Spanish Biomedical Research Centre in Cardiovascular Disease [CB16/11/00371, CB16/11/00333]
  6. Foundation for Applied Medical Research, Universidad de Navarra (Spain)
  7. La Caixa Banking Foundation [HR17-00247]

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Cardiovascular diseases are the leading cause of death globally. In recent years, there has been significant interest in studying extracellular vesicles (EVs) as potential biomarkers for the diagnosis and prognosis of chronic cardiovascular diseases. EVs play a crucial role in the pathological processes of cardiovascular remodeling, especially in vascular and valvular calcification.
Cardiovascular diseases (CVDs) are the first cause of death worldwide. In recent years, there has been great interest in the analysis of extracellular vesicles (EVs), including exosomes and microparticles, as potential mediators of biological communication between circulating cells/plasma and cells of the vasculature. Besides their activity as biological effectors, EVs have been also investigated as circulating/systemic biomarkers in different acute and chronic CVDs. In this review, the role of EVs as potential diagnostic and prognostic biomarkers in chronic cardiovascular diseases, including atherosclerosis (mainly, peripheral arterial disease, PAD), aortic stenosis (AS) and aortic aneurysms (AAs), will be described. Mechanistically, we will analyze the implication of EVs in pathological processes associated to cardiovascular remodeling, with special emphasis in their role in vascular and valvular calcification. Specifically, we will focus on the participation of EVs in calcium accumulation in the pathological vascular wall and aortic valves, involving the phenotypic change of vascular smooth muscle cells (SMCs) or valvular interstitial cells (IC) to osteoblast-like cells. The knowledge of the implication of EVs in the pathogenic mechanisms of cardiovascular remodeling is still to be completely deciphered but there are promising results supporting their potential translational application to the diagnosis and therapy of different CVDs.

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