Abstract
Nitric oxide (NO) is acknowledged as a vital intercellular messenger in multiple systems in the body. Medicine has focused on its functions and therapeutic applications for decades, especially in cardiovascular and nervous systems, and its role in immunological responses. This review was composed to demonstrate the prevalence of NO in components of the ocular system, including corneal cells and multiple cells in the retina. It discussed NO’s assistance during the immune, inflammation and wound-healing processes. NO is identified as a vascular endothelial relaxant that can alter the choroidal blood flow and prompt or suppress vascular changes in age-related macular degeneration and diabetes, as well as the blood supply to the optic nerve, possibly influencing the progression of glaucoma. It will provide a deeper understanding of the role of NO in ocular homeostasis, the delicate balance between overproduction or underproduction and the effect on the processes from aqueous outflow and subsequent intraocular pressure to axial elongation and the development of myopia. This review also recognized the research and investigation of therapies being developed to target the NO complex and treat various ocular diseases.
Highlights
Nitric oxide (NO) was first discovered in the 1770s by Joseph Priestly in England [1,2]
Knowledge of the tolerance and dosing of compounds as therapeutics has expanded, and NO is recognized as a potent vasodilator and endothelium-derived relaxing factor (EDRF) with the ability to impact multiple systems in the body [9,10,11,12,13,14,15,16,17]
These cultured cells with inactivated enzymes are somewhat comparable with what was observed in human conjunctival fibroblasts (HCF)—the expression of high levels of nitric oxide synthase (NOS)-2 mRNA compared to low NO production
Summary
Nitric oxide (NO) was first discovered in the 1770s by Joseph Priestly in England [1,2]. The endothelial (NOS-3) and neuronal (NOS-1) enzymes are calcium-dependent, which produce low levels of NO as a cell signaling molecule in resting cells [6,13,18] Another isoform of the enzyme is the inducible calcium-independent isoform (NOS-2) that is responsible for the release of NO during inflammation and is upregulated by a variety of extracellular stimuli, such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and LPS [6,13,18]. The same peroxynitrite pathway can alter the catalase activity, lowering the cell’s capacity to remove H2O2, perhaps prolonging the ROS-mediated signaling [27,28]. Included as well are the NO complex targeted treatments in development published in the literature as alternatives to the current available options
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