» Articles » PMID: 38001960

Therapeutic Potential of Antioxidants and Hybrid TEMPOL Derivatives in Ocular Neurodegenerative Diseases: A Glimpse into the Future

Overview
Journal Biomedicines
Date 2023 Nov 25
PMID 38001960
Authors
Affiliations
Soon will be listed here.
Abstract

Reactive oxygen species play a significant role in the pathogenesis of various ocular neurodegenerative diseases especially glaucoma, age-related macular degeneration (AMD), and ocular ischemic stroke. Increased oxidative stress and the accumulation of ROS have been implicated in the progression of these diseases. As a result, there has been growing interest in exploring potential therapeutic and prophylactic strategies involving exogenous antioxidants. In recent years, there have been significant advancements in the development of synthetic therapeutic antioxidants for targeting reactive oxygen species (ROS) in neurodegenerative diseases. One area of focus has been the development of hybrid TEMPOL derivatives. In the context of ocular diseases, the application of next-generation hybrid TEMPOL antioxidants may offer new avenues for neuroprotection. By targeting ROS and reducing oxidative stress in the retina and optic nerve, these compounds have the potential to preserve retinal ganglion cells and trabecular meshwork and protect against optic nerve damage, mitigating irreversible blindness associated with these diseases. This review seeks to highlight the potential impact of hybrid TEMPOL antioxidants and their derivatives on ocular neurodegenerative disorders.

Citing Articles

Tert-butyl hydroperoxide induces trabecular meshwork cells injury through ferroptotic cell death.

Yan X, Liu Q, Wu S, Fan X, Teng Y, Wang N J Cell Commun Signal. 2024; 18(3):e12050.

PMID: 39524143 PMC: 11544637. DOI: 10.1002/ccs3.12050.


The Role and Mechanism of Nicotinamide Riboside in Oxidative Damage and a Fibrosis Model of Trabecular Meshwork Cells.

Zeng Y, Lin Y, Yang J, Wang X, Zhu Y, Zhou B Transl Vis Sci Technol. 2024; 13(3):24.

PMID: 38546981 PMC: 10981432. DOI: 10.1167/tvst.13.3.24.

References
1.
Ung L, Pattamatta U, Carnt N, Wilkinson-Berka J, Liew G, White A . Oxidative stress and reactive oxygen species: a review of their role in ocular disease. Clin Sci (Lond). 2017; 131(24):2865-2883. DOI: 10.1042/CS20171246. View

2.
Kamel K, Farrell M, OBrien C . Mitochondrial dysfunction in ocular disease: Focus on glaucoma. Mitochondrion. 2017; 35:44-53. DOI: 10.1016/j.mito.2017.05.004. View

3.
Keller K, Acott T . The Juxtacanalicular Region of Ocular Trabecular Meshwork: A Tissue with a Unique Extracellular Matrix and Specialized Function. J Ocul Biol. 2013; 1(1):3. PMC: 3867143. View

4.
Chan E, Liu G, Dusting G . Redox mechanisms in pathological angiogenesis in the retina: roles for NADPH oxidase. Curr Pharm Des. 2015; 21(41):5988-98. DOI: 10.2174/1381612821666151029111127. View

5.
Baynes J, Thorpe S . Role of oxidative stress in diabetic complications: a new perspective on an old paradigm. Diabetes. 1999; 48(1):1-9. DOI: 10.2337/diabetes.48.1.1. View