Endothelial Extracellular Vesicles Produced by Senescent Cells: Pathophysiological Role in the Cardiovascular Disease Associated with all Types of Diabetes Mellitus.
Cardiovascular diseases
diabetes
endothelial senescence
epigenetic signals
extracellular vesicles
microvesicles
physiopathological mechanisms.
Journal
Current vascular pharmacology
ISSN: 1875-6212
Titre abrégé: Curr Vasc Pharmacol
Pays: United Arab Emirates
ID NLM: 101157208
Informations de publication
Date de publication:
2019
2019
Historique:
received:
24
05
2018
revised:
26
07
2018
accepted:
26
07
2018
pubmed:
21
8
2018
medline:
26
5
2020
entrez:
21
8
2018
Statut:
ppublish
Résumé
Endothelial senescence-associated with aging or induced prematurely in pathological situations, such as diabetes, is a first step in the development of Cardiovascular Disease (CVDs) and particularly inflammatory cardiovascular diseases. The main mechanism that links endothelial senescence and the progression of CVDs is the production of altered Extracellular Vesicles (EVs) by senescent endothelial cells among them, Microvesicles (MVs). MVs are recognized as intercellular signaling elements that play a key role in regulating tissue homeostasis. However, MVs produced by damage cell conveyed epigenetic signals, mainly involving microRNAs, which induce many of the injured responses in other vascular cells leading to the development of CVDs. Many studies strongly support that the quantification and characterization of the MVs released by senescent endothelial cells may be useful diagnostic tools in patients with CVDs, as well as a future therapeutic target for these diseases. In this review, we summarize the current knowledge linking senescence-associated MVs to the development of CVDs and discuss the roles of these MVs, in particular, in diabetic-associated increases the risk of CVDs.
Identifiants
pubmed: 30124156
pii: CVP-EPUB-92490
doi: 10.2174/1570161116666180820115726
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
447-454Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.