The indoleamine hormone, melatonin, is produced in the pineal gland and has an essential role in many physiological functions. The pineal gland is considered to be the most important organ for producing melatonin. Nevertheless, it is important to point out that the eye is also capable of producing melatonin, and has its own circadian rhythm in producing this hormone. Melatonin is mainly produced by a subpopulation of photoreceptors in a diurnal rhythm. Numerous in vitro and in vivo studies have shown the beneficial effects of melatonin in eye-related disorders. These diseases primarily affect retinal cells, highlighting the therapeutic potential of melatonin, especially in the retina. Melatonin's ability to regulate oxidative stress response pathways and modulate the expression of antioxidant genes makes it a promising candidate for mitigating retinal cell damage. Moreover, melatonin can modulate inflammatory pathways such as NF-кB and further reduce retinal damage, as well as affecting programmed cell death such as apoptosis and autophagy in retinal cells. Therefore, the goal of this review is to explore the ways in which melatonin protects retinal cells from damage and ischemia. We discuss the mechanisms involved in order to gain valuable understanding of the possible therapeutic applications of melatonin in protection of retinal cells and treatment of retinal disorders.
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http://dx.doi.org/10.1007/s00210-024-03575-w | DOI Listing |
Invest Ophthalmol Vis Sci
January 2025
Affiliated Eye Hospital of Nanchang University, Jiangxi Research Institute of Ophthalmology and Visual Science, Jiangxi Provincial Key Laboratory for Ophthalmology, Jiangxi Clinical Research Center for Ophthalmic Disease, Nanchang, China.
Purpose: This study aimed to investigate the role of SIRT4 in retinal protection, specifically its ability to mitigate excitotoxic damage to Müller glial cells through the regulation of mitochondrial dynamics and glutamate transporters (GLASTs).
Methods: A model of retinal excitatory neurotoxicity was established in mice. Proteins related to mitochondrial dynamics, GLAST, and SIRT4 were analyzed on days 0, 1, 3, and 5 following toxic injury.
Invest Ophthalmol Vis Sci
January 2025
School of Graduate, Dalian Medical University, Dalian City, China.
Purpose: To investigate the effect of Ca2+/calmodulin-dependent protein kinase II (CAMKII) δ subtypes (CAMK2D) on sodium iodate (NaIO3)-induced retinal degeneration in mice.
Methods: Bioinformatics analysis and Western blot experiments were used to screen the significantly differentially expressed genes in age-related macular degeneration (AMD) disease. CAMK2D knockdown and overexpression models were constructed by lentivirus (LV) infection of adult retinal pigment epithelial cell line-19 (ARPE-19) cells in vitro.
Glia
January 2025
Department of Ophthalmology, Bern University Hospital and Department of BioMedical Research, University of Bern, Bern, Switzerland.
Glia antigen-presenting cells (APCs) are pivotal regulators of immune surveillance within the retina, maintaining tissue homeostasis and promptly responding to insults. However, the intricate mechanisms underlying their local coordination and activation remain unclear. Our study integrates an animal model of retinal injury, retrospective analysis of human retinas, and in vitro experiments to gain insights into the crucial role of antigen presentation in neuroimmunology during retinal degeneration (RD), uncovering the involvement of various glial cells, notably Müller glia and microglia.
View Article and Find Full Text PDFIn Vitro Model
February 2024
iNOVA4Health, NOVA Medical School|Faculdade de Ciências Médicas, NMS|FCM, Universidade Nova de Lisboa, Rua Camara Pestana, 6, Lisbon, Portugal.
Purpose: Diabetic retinopathy (DR) is a complication of diabetes and a primary cause of visual impairment amongst working-age individuals. DR is a degenerative condition in which hyperglycaemia results in morphological and functional changes in certain retinal cells. Existing treatments mainly address the advanced stages of the disease, which involve vascular defects or neovascularization.
View Article and Find Full Text PDFJ Cell Sci
January 2025
Program in Molecular Medicine, University of Massachusetts Chan Medical School, Suite 213 Biotech II, 373 Plantation Street, Worcester MA 01605, USA.
In humans, inositol polyphosphate-5-phosphatase e (INPP5E) mutations cause retinal degeneration as part of Joubert and MORM syndromes and can also cause non-syndromic blindness. In mice, mutations cause a spectrum of brain, kidney, and other anomalies and prevent the formation of photoreceptor outer segments. To further explore the function of Inpp5e in photoreceptors, we generated conditional and inducible knockouts of mouse Inpp5e where the gene was deleted either during outer segment formation or after outer segments were fully formed.
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