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Article
Implications of Caspase 1/ Interleukin-1 Beta (IL-1β) Signaling and Hypoxia-Inducible Factor 1-Alpha (HIF-1α) on Diabetic Retinopathy Pathology.
Cureus
  • Drew Garber, Philadelphia College of Osteopathic Medicine
  • Shu Zhu, Philadelphia College of Osteopathic Medicine
Document Type
Article
Publication Date
7-1-2023
Abstract

Diabetic retinopathy (DR) is the leading cause of adult blindness and partial vision loss in modern society for hyperglycemic patients. Accordingly, new treatment options are imperative to the overall reduction of DR prevalence and the ongoing progression of already affected candidates. There are many diseases that are the direct result of specific inflammatory processes. In this literature, DR is looked at as a potential disease that can be alleviated by targeting caspase 1/ interleukin-1 beta (IL-1β), and hypoxia-inducible factor 1-alpha (HIF-1α) signaling pathways and reducing cytokine mobilization within retinal tissues. Caspase-1 is thought to be upregulated during retinal capillary degeneration and other ocular complications. Hypoxia-inducible factor 1-alpha (HIF-1α) is implicated in its role in neovascularization and cell apoptosis within a retinal cell line. Both of these proteins are shown to be significantly elevated in hyperglycemic and galactosemic mice and, when knocked out, seem to have the reverse effect, showing that there is room for potential non-invasive therapy involving these proteins in the future. Vascular endothelial growth factor-alpha (VEGF-A) is also examined as a main signaling protein involved in the manifestation of DR.

PubMed ID
37637673
Comments

This article was published in Cureus, Volume 15, Issue 7.

The published version is available at https://doi.org/10.7759/cureus.42479.

Copyright © 2023 Garber et al. CC BY 4.0.

Citation Information
Drew Garber and Shu Zhu. "Implications of Caspase 1/ Interleukin-1 Beta (IL-1β) Signaling and Hypoxia-Inducible Factor 1-Alpha (HIF-1α) on Diabetic Retinopathy Pathology." Cureus Vol. 15 Iss. 7 (2023)
Available at: http://works.bepress.com/shu_zhu/42/