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
. 2018 Jun 20;19(6):1816.
doi: 10.3390/ijms19061816.

Diabetic Retinopathy: Pathophysiology and Treatments

Affiliations
Review

Diabetic Retinopathy: Pathophysiology and Treatments

Wei Wang et al. Int J Mol Sci. .

Abstract

Diabetic retinopathy (DR) is the most common complication of diabetes mellitus (DM). It has long been recognized as a microvascular disease. The diagnosis of DR relies on the detection of microvascular lesions. The treatment of DR remains challenging. The advent of anti-vascular endothelial growth factor (VEGF) therapy demonstrated remarkable clinical benefits in DR patients; however, the majority of patients failed to achieve clinically-significant visual improvement. Therefore, there is an urgent need for the development of new treatments. Laboratory and clinical evidence showed that in addition to microvascular changes, inflammation and retinal neurodegeneration may contribute to diabetic retinal damage in the early stages of DR. Further investigation of the underlying molecular mechanisms may provide targets for the development of new early interventions. Here, we present a review of the current understanding and new insights into pathophysiology in DR, as well as clinical treatments for DR patients. Recent laboratory findings and related clinical trials are also reviewed.

Keywords: anti-VEGF; inflammation; laser treatment; retinal degeneration; vascular pathology.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
① Nesvacumab activates Tie-2 signaling and decreases vascular permeability by inhibiting Ang-2, an antagonist of Tie2. ② AKB-9778 activates Tie-2 signaling by inhibiting ③ VE-PTP, a negative regulator of Tie-2.

References

    1. Romero-Aroca P., Baget-Bernaldiz M., Pareja-Rios A., Lopez-Galvez M., Navarro-Gil R., Verges R. Diabetic macular edema pathophysiology: Vasogenic versus inflammatory. J. Diabetes Res. 2016;2016:2156273. doi: 10.1155/2016/2156273. - DOI - PMC - PubMed
    1. Gonzalez V.H., Campbell J., Holekamp N.M., Kiss S., Loewenstein A., Augustin A.J., Ma J., Ho A.C., Patel V., Whitcup S.M., et al. Early and long-term responses to anti-vascular endothelial growth factor therapy in diabetic macular edema: Analysis of protocol I data. Am. J. Ophthalmol. 2016;172:72–79. doi: 10.1016/j.ajo.2016.09.012. - DOI - PubMed
    1. Brownlee M. The pathobiology of diabetic complications: A unifying mechanism. Diabetes. 2005;54:1615–1625. doi: 10.2337/diabetes.54.6.1615. - DOI - PubMed
    1. Bek T. Diameter changes of retinal vessels in diabetic retinopathy. Curr. Diabetes Rep. 2017;17:82. doi: 10.1007/s11892-017-0909-9. - DOI - PubMed
    1. Naruse K., Nakamura J., Hamada Y., Nakayama M., Chaya S., Komori T., Kato K., Kasuya Y., Miwa K., Hotta N. Aldose reductase inhibition prevents glucose-induced apoptosis in cultured bovine retinal microvascular pericytes. Exp. Eye Res. 2000;71:309–315. doi: 10.1006/exer.2000.0882. - DOI - PubMed

MeSH terms