Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 May 25:13:816400.
doi: 10.3389/fendo.2022.816400. eCollection 2022.

Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy

Jing Yang  1   2   3   4 , Zhangsuo Liu  2   3   4   5
Affiliations
Review

Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy

Jing Yang et al. Front Endocrinol (Lausanne). .

Abstract

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.

Keywords: CircRNAs; cellular crosstalk; diabetic endothelial dysfunction; diabetic nephropathy (DN); diabetic retinopathy (DR); exosomes.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Schematic illustration of the pathological mechanisms of endothelial dysfunction in diabetic retinopathy and diabetic nephropathy.
See this image and copyright information in PMC

References

    1. Cho NH, Shaw JE, Karuranga S, Huang Y, da Rocha Fernandes JD, Ohlrogge AW, et al. . IDF Diabetes Atlas: Global Estimates of Diabetes Prevalence for 2017 and Projections for 2045. Diabetes Res Clin Pract (2018) 138:271–81. doi: 10.1016/j.diabres.2018.02.023 - DOI - PubMed
    1. Wild S, Roglic G, Green A, Sicree R, King H. Global Prevalence of Diabetes: Estimates for the Year 2000 and Projections for 2030. Diabetes Care (2004) 27(5):1047–53. doi: 10.2337/diacare.27.5.1047 - DOI - PubMed
    1. Shaw JE, Sicree RA, Zimmet PZ. Global Estimates of the Prevalence of Diabetes for 2010 and 2030. Diabetes Res Clin Pract (2010) 87(1):4–14. doi: 10.1016/j.diabres.2009.10.007 - DOI - PubMed
    1. Zhang P, Zhang X, Brown J, Vistisen D, Sicree R, Shaw J, et al. . Global Healthcare Expenditure on Diabetes for 2010 and 2030. Diabetes Res Clin Pract (2010) 87(3):293–301. doi: 10.1016/j.diabres.2010.01.026 - DOI - PubMed
    1. Broekhuizen LN, Lemkes BA, Mooij HL, Meuwese MC, Verberne H, Holleman F, et al. . Effect of Sulodexide on Endothelial Glycocalyx and Vascular Permeability in Patients with Type 2 Diabetes Mellitus. Diabetologia (2010) 53(12):2646–55. doi: 10.1007/s00125-010-1910-x - DOI - PMC - PubMed

Publication types

MeSH terms

Substances