The recognition of the importance of overweigh / obesity
and metabolic syndrome as leading risk factor for diabetes and
cardiovascular (CV) complications has greatly increased within
last decades. Endothelial dysfunction mediating the diabetic
complications associates with several important mechanisms, one
of which is secretion of extracellular microparticles (MPs) by
activated or apoptotic endothelial cells. MPs coordinate wide
spectrum
biological
processes,
i.e.
angiogenesis,
neovascularization, cell growth / differentiation, proliferation,
coagulation, and they are involved in the epigenetic regulation of
post-processing that is essential for phenotype modification, tissue
repair, cell death, malignancy, and immunity. The commentary is
discussed the role of impaired balance between number of both
immune subsets of endothelial MPs in CV events development
among dysmetabolic subjects. It has revealed that increased
numbers of apoptotic MPs, as well as decreased numbers of MPs
derived from activated endothelial cells aggravate endothelial
damage and contribute to the continuously deteriorating
endothelial damage leading to diabetes-related complications.
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“Impaired Phenotype” of Endothelial Cell-Derived Microparticles: Causality Factor Contributed the "Vascular Competence" in Diabetes and Metabolic Syndrome?
Alexander E Berezin*
Corresponding Author: Alexander E Berezin*
Received: Apr 11, 2016
Accepted: May 10, 2016
Published: May 13, 2016
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DOI: N/A
Abstract
Alexander E Berezin (2016), “Impaired Phenotype” of Endothelial Cell-Derived Microparticles: Causality Factor Contributed the
“Vascular Competence” in Diabetes and Metabolic Syndrome? Diabetes Res Treat Open Access 3: 133
Copyright:
Copyright: © 2016 DRTOA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, Version 3.0, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and source are credited.
use, distribution, and reproduction in any medium, provided the original author and source are credited.
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