Under OS, the activation of this immune pathway aims to repair tissue homeostasis. The retina is endowed with an efficient innate immune system that activates three essential pathways: migration of microglia, stimulation of the complement system, and inflammasome assembly in the retinal pigment epithelium (RPE).įor this response, retinal cells are endowed with a variety of immune receptors and mediators such as microbial sensors (TLRs), NOD‐like receptors‐NLRs, RIG‐1 like helicases, cytokines, chemokines, and complement components all these players are in charge to help the cells to eliminate the insult. It is noteworthy that products of the oxidation of docosahexaenoic acid (DHA)–containing lipids (CEP‐EPs) are observed at elevated levels both in the eyes and in serum of AMD patients compared with age‐matched controlsĪnd are reported as activators of Toll‐like receptor 2 (TLR2) in AMD and in other retinal diseases where ROS exert a role in pathology.
High ROS levels can cause lipid peroxidation which is found at elevated amounts in the photoreceptor cell membrane. Moreover, OS is thought to induce a deficiency of cone photoreceptors in rare inherited retinopathies. Age‐related macular degeneration (AMD), diabetic retinopathy (DR), and glaucoma are ocular disorders that can lead to visual loss, and for which the involvement of ROS has been evoked. The retina is susceptible to OS due to its elevated oxygen consumption and exposure to visible light, which can potentiate cellular damage caused by ROS.Įlevated OS levels determine dramatic changes that lead to visual impairment. Retinal cell survival involves redox signaling and a balance between reactive oxygen species (ROS) and antioxidant scavengers to counteract OS injury. Oxidative stress (OS) plays a major role in the neurodegenerative process. Antiapoptotic effects are also involved however, the protective mechanisms exerted by taurine against retinal damage remain to be further investigated. In particular, it has been demonstrated to improve retinal reduced glutathione, malondialdehyde, superoxide dismutase, and catalase activities. The mechanism by which taurine supplementation acts is mainly related to the reduction of oxidative stress. Increasing data indicate that taurine may be effective in slowing down the progression of degenerative retinal diseases, thus suggesting that taurine can be a promising candidate for the prevention or as adjuvant treatment of these diseases. This review will discuss the impact of oxidative stress in retinal neurodegenerative diseases and the potential strategies for avoiding or counteracting oxidative damage in retinal tissues, with a specific focus on taurine. Different approaches using nutraceuticals resulted in protective effects in these disorders. Indeed, it is well known that oxidative stress is one of the leading causes of retinal degenerative diseases.
Retinal disorders are leading causes of blindness and are due to an imbalance between reactive oxygen species and antioxidant scavenger (in favor of pro‐oxidant species) or a disruption of redox signaling and control.
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