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Academic literature on the topic 'Inflammation, retinitis pigmentosa'
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Journal articles on the topic "Inflammation, retinitis pigmentosa"
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Jadeja, Ravirajsinh N., and Pamela M. Martin. "Oxidative Stress and Inflammation in Retinal Degeneration." Antioxidants 10, no. 5 (May 17, 2021): 790. http://dx.doi.org/10.3390/antiox10050790.
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Inflammation and oxidative stress play prominent roles in the pathogenesis of many degenerative diseases of the retina, such as age-related macular degeneration (AMD), diabetic retinopathy (DR), retinal vein occlusion, and retinitis pigmentosa [...]
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Napoli, Debora, Martina Biagioni, Federico Billeri, Beatrice Di Marco, Noemi Orsini, Elena Novelli, and Enrica Strettoi. "Retinal Pigment Epithelium Remodeling in Mouse Models of Retinitis Pigmentosa." International Journal of Molecular Sciences 22, no. 10 (May 20, 2021): 5381. http://dx.doi.org/10.3390/ijms22105381.
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In retinitis pigmentosa (RP), one of many possible genetic mutations causes rod degeneration, followed by cone secondary death leading to blindness. Accumulating evidence indicates that rod death triggers multiple, non-cell-autonomous processes, which include oxidative stress and inflammation/immune responses, all contributing to cone demise. Inflammation relies on local microglia and recruitment of immune cells, reaching the retina through breakdowns of the inner blood retinal barrier (iBRB). Leakage in the inner retina vasculature suggests similarly altered outer BRB, formed by junctions between retinal pigment epithelium (RPE) cells, which are crucial for retinal homeostasis, immune response, and privilege. We investigated the RPE structural integrity in three models of RP (rd9, rd10, and Tvrm4 mice) by immunostaining for zonula occludens-1 (ZO-1), an essential regulatory component of tight junctions. Quantitative image analysis demonstrated discontinuities in ZO-1 profiles in all mutants, despite different degrees of photoreceptor loss. ZO-1 interruption zones corresponded to leakage of in vivo administered, fluorescent dextran through the choroid-RPE interface, demonstrating barrier dysfunction. Dexamethasone, administered to rd10 mice for rescuing cones, also rescued RPE structure. Thus, previously undetected, stereotyped abnormalities occur in the RPE of RP mice; pharmacological targeting of inflammation supports a feedback loop leading to simultaneous protection of cones and the RPE.
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Karlen, Sarah J., Eric B. Miller, and Marie E. Burns. "Microglia Activation and Inflammation During the Death of Mammalian Photoreceptors." Annual Review of Vision Science 6, no. 1 (September 15, 2020): 149–69. http://dx.doi.org/10.1146/annurev-vision-121219-081730.
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Photoreceptors are highly specialized sensory neurons with unique metabolic and physiological requirements. These requirements are partially met by Müller glia and cells of the retinal pigment epithelium (RPE), which provide essential metabolites, phagocytose waste, and control the composition of the surrounding microenvironment. A third vital supporting cell type, the retinal microglia, can provide photoreceptors with neurotrophic support or exacerbate neuroinflammation and hasten neuronal cell death. Understanding the physiological requirements for photoreceptor homeostasis and the factors that drive microglia to best promote photoreceptor survival has important implications for the treatment and prevention of blinding degenerative diseases like retinitis pigmentosa and age-related macular degeneration.
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Gallenga, Carla Enrica, Maria Lonardi, Sofia Pacetti, Sara Silvia Violanti, Paolo Tassinari, Francesco Di Virgilio, Mauro Tognon, and Paolo Perri. "Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa." Antioxidants 10, no. 6 (May 26, 2021): 848. http://dx.doi.org/10.3390/antiox10060848.
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Retinitis pigmentosa (RP) is an inherited retinopathy. Nevertheless, non-genetic biological factors play a central role in its pathogenesis and progression, including inflammation, autophagy and oxidative stress. The retina is particularly affected by oxidative stress due to its high metabolic rate and oxygen consumption as well as photosensitizer molecules inside the photoreceptors being constantly subjected to light/oxidative stress, which induces accumulation of ROS in RPE, caused by damaged photoreceptor’s daily recycling. Oxidative DNA damage is a key regulator of microglial activation and photoreceptor degeneration in RP, as well as mutations in endogenous antioxidant pathways involved in DNA repair, oxidative stress protection and activation of antioxidant enzymes (MUTYH, CERKL and GLO1 genes, respectively). Moreover, exposure to oxidative stress alters the expression of micro-RNA (miRNAs) and of long non-codingRNA (lncRNAs), which might be implicated in RP etiopathogenesis and progression, modifying gene expression and cellular response to oxidative stress. The upregulation of the P2X7 receptor (P2X7R) also seems to be involved, causing pro-inflammatory cytokines and ROS release by macrophages and microglia, contributing to neuroinflammatory and neurodegenerative progression in RP. The multiple pathways analysed demonstrate that oxidative microglial activation may trigger the vicious cycle of non-resolved neuroinflammation and degeneration, suggesting that microglia may be a key therapy target of oxidative stress in RP.
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Viringipurampeer, Ishaq A., Abu E. Bashar, Cheryl Y. Gregory-Evans, Orson L. Moritz, and Kevin Gregory-Evans. "Targeting Inflammation in Emerging Therapies for Genetic Retinal Disease." International Journal of Inflammation 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/581751.
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Genetic retinal diseases such as age-related macular degeneration and monogenic diseases such as retinitis pigmentosa account for some of the commonest causes of blindness in the developed world. Diverse genetic abnormalities and environmental causes have been implicated in triggering multiple pathological mechanisms such as oxidative stress, lipofuscin deposits, neovascularisation, and programmed cell death. In recent years, inflammation has also been highlighted although whether inflammatory mediators play a central role in pathogenesis or a more minor secondary role has yet to be established. Despite this, numerous interventional studies, particularly targeting the complement system, are underway with the promise of novel therapeutic strategies for these important blinding conditions.
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Woude, Logan Vander, Ramak Roohipour, and Gibran Syed Khurshid. "Phthisis Bulbi in a Retinitis Pigmentosa Patient after Argus II Implantation." Case Reports in Ophthalmological Medicine 2020 (August 17, 2020): 1–4. http://dx.doi.org/10.1155/2020/5608058.
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Purpose. To report a previously unreported complication of phthisis after Argus II prosthesis implantation in a retinitis pigmentosa (RP) patient. Case. A 61-year-old male with advanced RP presented to the retina clinic. The patient had a history of vitrectomy in both eyes (OU) in Cuba in 1996. Pre-op visual acuity (VA) was no light perception (NLP) in the right eye and light perception (LP) in the left eye. The patient met the criteria for Argus II implantation and elected to proceed with surgery in his left eye in December 2017. The surgical implantation of the Argus II was successful without any complications. On postoperative day 1, his VA was stable at LP. He was satisfied with his ambulatory vision after the electrodes were turned on. Four months after surgery, the patient was complaining of aching pain; he was found to have preseptal cellulitis and was started on antibiotics. This swelling improved over two weeks, but when the patient returned, he had a two mm hyphema associated with mild ocular inflammation without an inciting event or reason on exam. The hyphema was treated and resolved after two weeks. However, one month after the hyphema resolved, at postoperative month six, the patient’s vision in his left eye became NLP and began to demonstrate phthisical changes, including hypotony, Descemet membrane folds, and a vascular posterior capsular membrane. Discussion. The theoretical causes of phthisis bulbi after Argus II implantation include fibrous downgrowth, ciliary shut down due to immune reaction, inflammation, or trauma. While the cause of phthisis in this Argus patient is not certain and possibly multifactorial, it is important to note that phthisis is a possible complication of an Argus II implant, as this patient had no other obvious insult or reason for the phthisical change.
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Hong, Yingying, Hongzhe Li, Yang Sun, and Yinghong Ji. "A Review of Complicated Cataract in Retinitis Pigmentosa: Pathogenesis and Cataract Surgery." Journal of Ophthalmology 2020 (December 21, 2020): 1–14. http://dx.doi.org/10.1155/2020/6699103.
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Retinitis pigmentosa (RP) is a set of inherited retinal degenerative diseases that affect photoreceptor and retinal pigment epithelial cells (RPEs), possibly associated with some ocular complications, including cataract. The complicated cataract formation is most likely the result of RP-related inflammation response, and the most common morphology category is posterior subcapsular cataract (PSC). Despite the absence of curative pharmacologic treatment, phacoemulsification with intraocular lens implantation to deal with opacification in the lens is preferred due to the considerable visual outcomes. However, the incidence of intraocular and postoperative complications is higher in RP patients than those without, including intraoperative phototoxic retinal damage, posterior capsular opacification (PCO), capsular contraction syndrome (CCS), pseudophakic cystoid macular edema (PCME), increased postoperative intraocular pressure (IOP), and intraocular lens (IOL) dislocation. Hence, it needs much attention to surgery progress and close follow-up. In this review, we discuss the current understanding of RP patients with complicated cataracts from morphology to potential pathogenesis to cataract surgical procedure and provide a concise description and the recommended management of related surgery complications to broaden the knowledge and lower the latent risks to yield better clinical outcomes.
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Cantó, Antolín, Javier Martínez-González, Inmaculada Almansa, Rosa López-Pedrajas, Vicente Hernández-Rabaza, Teresa Olivar, and María Miranda. "Time-Course Changes in Oxidative Stress and Inflammation in the Retinas of rds Mice: A Retinitis Pigmentosa Model." Antioxidants 11, no. 10 (September 29, 2022): 1950. http://dx.doi.org/10.3390/antiox11101950.
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(1) Background: Retinitis pigmentosa (RP) is characterized by progressive photoreceptor death. A Prph2Rd2 or an rds mouse is an RP model that closely reflects human RP. The objective of this study was to investigate the relationship of rod and cone death with oxidative stress and inflammation in rds mice. (2) Methods: The retinas of control and rds mice on postnatal days (PN) 11, 17, 21, 28, 35, and 42 were used. Oxidative damage to macromolecules, glutathione (GSH and GSSG), GSH synthesis enzymes, glial fibrillar acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba1), and cluster of differentiation 68 (CD68) was studied. (3) Results: The time sequence of oxidative stress and inflammation changes in rds mice occurs as follows: (i) At PN11, there is a small increase in photoreceptor death and in the microglial cells; (ii) at PN17, damage to the macromolecules is observed; (iii) at PN21, the maximum photoreceptor death rate is detected and there is an increase in GSH-GSSG and GFAP; (iv) at PN21, the microglial cells are activated; and(v) at PN28, there is a decrease in GSH synthesis enzymes. (4) Conclusions: These findings contribute to the understanding of RP physiopathology and help us to understand whether oxidative stress and inflammation are therapeutic targets. These findings contribute to our understanding that, in RP, oxidative stress and inflammation evolution and their relationship are time-dependent. In this sense, it is important to highlight that both processes are potential therapeutic targets in this disease.
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Li, Xing, Reem Hasaballah Alhasani, Yanqun Cao, Xinzhi Zhou, Zhiming He, Zhihong Zeng, Niall Strang, and Xinhua Shu. "Gypenosides Alleviate Cone Cell Death in a Zebrafish Model of Retinitis Pigmentosa." Antioxidants 10, no. 7 (June 29, 2021): 1050. http://dx.doi.org/10.3390/antiox10071050.
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Retinitis pigmentosa (RP) is a group of visual disorders caused by mutations in over 70 genes. RP is characterized by initial degeneration of rod cells and late cone cell death, regardless of genetic abnormality. Rod cells are the main consumers of oxygen in the retina, and after the death of rod cells, the cone cells have to endure high levels of oxygen, which in turn leads to oxidative damage and cone degeneration. Gypenosides (Gyp) are major dammarane-type saponins of Gynostemma pentaphyllum that are known to reduce oxidative stress and inflammation. In this project we assessed the protective effect of Gyp against cone cell death in the rpgrip1 mutant zebrafish, which recapitulate the classical pathological features found in RP patients. Rpgrip1 mutant zebrafish were treated with Gyp (50 µg/g body weight) from two-months post fertilization (mpf) until 6 mpf. Gyp treatment resulted in a significant decrease in cone cell death compared to that of untreated mutant zebrafish. A markedly low level of reactive oxygen species and increased expression of antioxidant genes were detected in Gyp-incubated mutant zebrafish eyes compared to that of untreated mutant zebrafish. Similarly, the activities of catalase and superoxide dismutase and the level of glutathione were significantly increased in Gyp-treated mutant zebrafish eyes compared to that of untreated mutant zebrafish. Gyp treatment also decreased endoplasmic reticulum stress in rpgrip1 mutant eyes. Expression of proinflammatory cytokines was also significantly decreased in Gyp-treated mutant zebrafish eyes compared to that of untreated mutant zebrafish. Network pharmacology analysis demonstrated that the promotion of cone cell survival by Gyp is possibly mediated by multiple hub genes and associated signalling pathways. These data suggest treatment with Gyp will benefit RP patients.
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Olivares-González, Lorena, Sheyla Velasco, Isabel Campillo, and Regina Rodrigo. "Retinal Inflammation, Cell Death and Inherited Retinal Dystrophies." International Journal of Molecular Sciences 22, no. 4 (February 20, 2021): 2096. http://dx.doi.org/10.3390/ijms22042096.
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Inherited retinal dystrophies (IRDs) are a group of retinal disorders that cause progressive and severe loss of vision because of retinal cell death, mainly photoreceptor cells. IRDs include retinitis pigmentosa (RP), the most common IRD. IRDs present a genetic and clinical heterogeneity that makes it difficult to achieve proper treatment. The progression of IRDs is influenced, among other factors, by the activation of the immune cells (microglia, macrophages, etc.) and the release of inflammatory molecules such as chemokines and cytokines. Upregulation of tumor necrosis factor alpha (TNFα), a pro-inflammatory cytokine, is found in IRDs. This cytokine may influence photoreceptor cell death. Different cell death mechanisms are proposed, including apoptosis, necroptosis, pyroptosis, autophagy, excessive activation of calpains, or parthanatos for photoreceptor cell death. Some of these cell death mechanisms are linked to TNFα upregulation and inflammation. Therapeutic approaches that reduce retinal inflammation have emerged as useful therapies for slowing down the progression of IRDs. We focused this review on the relationship between retinal inflammation and the different cell death mechanisms involved in RP. We also reviewed the main anti-inflammatory therapies for the treatment of IRDs.
Dissertations / Theses on the topic "Inflammation, retinitis pigmentosa"
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Bacherini, Daniela, Stanislao Rizzo, Gianni Virgili, Andrea Sodi, Lorenzo Vannozzi, Francesco Annunziato, Laura Maggi, and Francesco Liotta. "Ruolo dell’infiammazione nella retinite pigmentosa: marcatori di flogosi nell’umor acqueo di pazienti affetti." Doctoral thesis, 2019. http://hdl.handle.net/2158/1155162.
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BIAGIONI, MARTINA. "Fighting inflammation to save cones: anti-inflammatory approaches to slow down cone degeneration in a mouse model of retinitis pigmentosa." Doctoral thesis, 2019. http://hdl.handle.net/2158/1151621.
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The term Retinitis Pigmentosa (RP) defines a group of inherited dystrophies characterized by progressive degeneration of photoreceptors (PRs) and abnormalities in retinal pigment epithelium (RPE). In typical RP, primary degeneration of rods is followed by secondary death of cones. Affected individuals exhibit initial night blindness and constricted visual field, while central vision is eventually lost later, as cone cells degenerate. Unfortunately, there is no cure for RP.
An important concept of RP pathophysiology is the biological link(s) between rod and cone death in this disease, where mutations are usually rod-specific and cones, genetically intact, degenerate as a consequence of a bystander effect. To note, the main cause of clinically significant vision loss is associated with cone, rather than with rod death. Although cones represent less than 5% of all PRs in the retina of most mammals, their role on human vision is crucial and their degeneration leads to a condition of irreversible vision loss. Survival of still-functioning cones following rod death enables patients with a night-blindness disease to lead normal lives for some time (Shelley et al., 2009).
Previous studies of our laboratory and based on the rd10 mouse model of human RP demonstrated with molecular tools that inflammation emerges as a relevant component of RP, overcoming any other biological process expected to occur in this pathology. Here, we hypothesized that cones, non-primarily affected by the disease-causing mutation and long lasting with respect to rods, may suffer from side effects of such inflammatory process and finally die out. In this study, we employed a protocol of synthetic steroid administration to test the hypothesis that counteracting retinal inflammation concomitantly to the acute phase of PR degeneration may improve cone fate. Indeed, we demonstrated that systemic Dexamethasone treatment resulted in decreased inflammatory response at retinal level and this event was associated to improved cone survival and preservation of visual acuity in rd10 mice. Subsequently, we postulated that different classes of Mononuclear Phagocytes (MPs, such as microglia and monocytes-derived macrophages, primarily involved in the inflammatory response) played different roles in the chronic, noxious inflammatory response found at retinal level. The particular role of the CCL2 chemokine was assessed.
Altogether, our findings suggest a link between local retinal inflammation and worsening of cone fate, opening the perspective of slowing down retinal decay and vision loss in RP by using anti-inflammatory strategies.