Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy
Diabetic nephropathy (DN) and diabetic retinopathy (DR) are microvascular complications of diabetes. Microvascular endothelial cells are thought to be the major targets of hyperglycemic injury. In diabetic microvasculature, the intracellular hyperglycemia causes damages to the vascular endothelium,...
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Published in | Frontiers in endocrinology (Lausanne) Vol. 13; p. 816400 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
25.05.2022
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Subjects | |
Online Access | Get full text |
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Summary: | Diabetic nephropathy (DN) and diabetic retinopathy (DR) are microvascular complications of diabetes. Microvascular endothelial cells are thought to be the major targets of hyperglycemic injury. In diabetic microvasculature, the intracellular hyperglycemia causes damages to the vascular endothelium, via multiple pathophysiological process consist of inflammation, endothelial cell crosstalk with podocytes/pericytes and exosomes. In addition, DN and DR diseases development are involved in several critical regulators including the cell adhesion molecules (CAMs), the vascular endothelial growth factor (VEGF) family and the Notch signal. The present review attempts to gain a deeper understanding of the pathogenesis complexities underlying the endothelial dysfunction in diabetes diabetic and retinopathy, contributing to the development of new mechanistic therapeutic strategies against diabetes-induced microvascular endothelial dysfunction. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 This article was submitted to Diabetes: Molecular Mechanisms, a section of the journal Frontiers in Endocrinology Edited by: Ana Stancic, University of Belgrade, Serbia Reviewed by: Jelena Kotur-Stevuljević, University of Belgrade, Serbia; Hu Huang, University of Missouri, United States |
ISSN: | 1664-2392 1664-2392 |
DOI: | 10.3389/fendo.2022.816400 |