Pub Date : 2024-01-31DOI: 10.3389/fopht.2024.1346361
Samar A. Al-Swailem, Hind M. Alkatan, Huda Saif AlDhaheri, S. AlHilali, Azza M. Y. Maktabi
To report clinical features and treatment outcome of three cases with isolated corneal intraepithelial neoplasia (CIN).This case series presents 3 patients with isolated CIN. Data collected included, presenting signs and symptoms including vision, anterior segment examination, medical and surgical outcomes and signs and symptoms at lost post-treatment visit.Case 1 was a 45-year-old male who presented with an isolated grayish amoeboid corneal lesion which was excised with alcohol assisted epitheliectomy, he also received 6 cycles of topical mitomycin C (MMC) 0.02% and one injection of interferon alfa-2b with no recurrence during the 10-year follow-up period. Case 2 was 78-year-old male referred for a suspicious white corneal lesion which was completely excised, the patient also received 6 subconjunctival injections of interferon alpha-2b. However, the lesion recurred at 2.5-years post-treatment. Case 3 was a 63-year-old male patient who presented with an isolated corneal lesion that was excised using alcohol-assisted epitheliectomy, patient received four cycles of topical 5-fluorouracil with no recurrence at last follow-up visit at 6 months.Isolated corneal intraepithelial neoplasia (CIN) is a rare entity with few reported cases in the literature. In this case series, we report long and short-term management outcomes of combined surgical and medical therapy for isolated CIN.
{"title":"Case report: Clinical features and management outcomes of isolated corneal intraepithelial neoplasia","authors":"Samar A. Al-Swailem, Hind M. Alkatan, Huda Saif AlDhaheri, S. AlHilali, Azza M. Y. Maktabi","doi":"10.3389/fopht.2024.1346361","DOIUrl":"https://doi.org/10.3389/fopht.2024.1346361","url":null,"abstract":"To report clinical features and treatment outcome of three cases with isolated corneal intraepithelial neoplasia (CIN).This case series presents 3 patients with isolated CIN. Data collected included, presenting signs and symptoms including vision, anterior segment examination, medical and surgical outcomes and signs and symptoms at lost post-treatment visit.Case 1 was a 45-year-old male who presented with an isolated grayish amoeboid corneal lesion which was excised with alcohol assisted epitheliectomy, he also received 6 cycles of topical mitomycin C (MMC) 0.02% and one injection of interferon alfa-2b with no recurrence during the 10-year follow-up period. Case 2 was 78-year-old male referred for a suspicious white corneal lesion which was completely excised, the patient also received 6 subconjunctival injections of interferon alpha-2b. However, the lesion recurred at 2.5-years post-treatment. Case 3 was a 63-year-old male patient who presented with an isolated corneal lesion that was excised using alcohol-assisted epitheliectomy, patient received four cycles of topical 5-fluorouracil with no recurrence at last follow-up visit at 6 months.Isolated corneal intraepithelial neoplasia (CIN) is a rare entity with few reported cases in the literature. In this case series, we report long and short-term management outcomes of combined surgical and medical therapy for isolated CIN.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"271 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140472884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-31DOI: 10.3389/fopht.2024.1355379
Michael Landowski, Purnima Gogoi, S. Ikeda, A. Ikeda
Aging is the most significant risk factor for age-related diseases in general, which is true for age-related diseases in the eye including age-related macular degeneration (AMD). Therefore, in order to identify potential therapeutic targets for these diseases, it is crucial to understand the normal aging process and how its mis-regulation could cause age-related diseases at the molecular level. Recently, abnormal lipid metabolism has emerged as one major aspect of age-related symptoms in the retina. Animal models provide excellent means to identify and study factors that regulate lipid metabolism in relation to age-related symptoms. Central to this review is the role of transmembrane protein 135 (TMEM135) in the retina. TMEM135 was identified through the characterization of a mutant mouse strain exhibiting accelerated retinal aging and positional cloning of the responsible mutation within the gene, indicating the crucial role of TMEM135 in regulating the normal aging process in the retina. Over the past decade, the molecular functions of TMEM135 have been explored in various models and tissues, providing insights into the regulation of metabolism, particularly lipid metabolism, through its action in multiple organelles. Studies indicated that TMEM135 is a significant regulator of peroxisomes, mitochondria, and their interaction. Here, we provide an overview of the molecular functions of TMEM135 which is crucial for regulating mitochondria, peroxisomes, and lipids. The review also discusses the age-dependent phenotypes in mice with TMEM135 perturbations, emphasizing the importance of a balanced TMEM135 function for the health of the retina and other tissues including the heart, liver, and adipose tissue. Finally, we explore the potential roles of TMEM135 in human age-related retinal diseases, connecting its functions to the pathobiology of AMD.
{"title":"Roles of transmembrane protein 135 in mitochondrial and peroxisomal functions - implications for age-related retinal disease.","authors":"Michael Landowski, Purnima Gogoi, S. Ikeda, A. Ikeda","doi":"10.3389/fopht.2024.1355379","DOIUrl":"https://doi.org/10.3389/fopht.2024.1355379","url":null,"abstract":"Aging is the most significant risk factor for age-related diseases in general, which is true for age-related diseases in the eye including age-related macular degeneration (AMD). Therefore, in order to identify potential therapeutic targets for these diseases, it is crucial to understand the normal aging process and how its mis-regulation could cause age-related diseases at the molecular level. Recently, abnormal lipid metabolism has emerged as one major aspect of age-related symptoms in the retina. Animal models provide excellent means to identify and study factors that regulate lipid metabolism in relation to age-related symptoms. Central to this review is the role of transmembrane protein 135 (TMEM135) in the retina. TMEM135 was identified through the characterization of a mutant mouse strain exhibiting accelerated retinal aging and positional cloning of the responsible mutation within the gene, indicating the crucial role of TMEM135 in regulating the normal aging process in the retina. Over the past decade, the molecular functions of TMEM135 have been explored in various models and tissues, providing insights into the regulation of metabolism, particularly lipid metabolism, through its action in multiple organelles. Studies indicated that TMEM135 is a significant regulator of peroxisomes, mitochondria, and their interaction. Here, we provide an overview of the molecular functions of TMEM135 which is crucial for regulating mitochondria, peroxisomes, and lipids. The review also discusses the age-dependent phenotypes in mice with TMEM135 perturbations, emphasizing the importance of a balanced TMEM135 function for the health of the retina and other tissues including the heart, liver, and adipose tissue. Finally, we explore the potential roles of TMEM135 in human age-related retinal diseases, connecting its functions to the pathobiology of AMD.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"187 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140478396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-29DOI: 10.3389/fopht.2023.1349525
M. Vaphiades
A 26-year-old man developed visual snow syndrome (VSS) after consuming a little less than half of a delta-8 gummy (estimated at 4 mg of delta-8 tetrahydrocannabinol). Secondary VSS and hallucinogen-persisting perception disorder (HPPD) are discussed, and clinicians who evaluate patients with VS and VSS should ask about delta-8 gummies as an etiology of secondary VSS.
{"title":"Delta-8 gummies causing visual snow: a case report","authors":"M. Vaphiades","doi":"10.3389/fopht.2023.1349525","DOIUrl":"https://doi.org/10.3389/fopht.2023.1349525","url":null,"abstract":"A 26-year-old man developed visual snow syndrome (VSS) after consuming a little less than half of a delta-8 gummy (estimated at 4 mg of delta-8 tetrahydrocannabinol). Secondary VSS and hallucinogen-persisting perception disorder (HPPD) are discussed, and clinicians who evaluate patients with VS and VSS should ask about delta-8 gummies as an etiology of secondary VSS.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"63 34","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140486661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-17DOI: 10.3389/fopht.2023.1309836
A. Vallbona-Garcia, Patrick J. Lindsey, Rick Kamps, A. Stassen, Nhan Nguyen, F. van Tienen, Ilse H. J. Hamers, Rianne Hardij, Marike W. van Gisbergen, Birke J. Benedikter, Irenaeus F. M. de Coo, C. A. Webers, Theo G. M. F. Gorgels, H. J. Smeets
Primary open-angle glaucoma (POAG) is a characteristic optic neuropathy, caused by degeneration of the optic nerve-forming neurons, the retinal ganglion cells (RGCs). High intraocular pressure (IOP) and aging have been identified as major risk factors; yet the POAG pathophysiology is not fully understood. Since RGCs have high energy requirements, mitochondrial dysfunction may put the survivability of RGCs at risk. We explored in buffy coat DNA whether mtDNA variants and their distribution throughout the mtDNA could be risk factors for POAG.The mtDNA was sequenced from age- and sex-matched study groups, being high tension glaucoma (HTG, n=71), normal tension glaucoma patients (NTG, n=33), ocular hypertensive subjects (OH, n=7), and cataract controls (without glaucoma; n=30), all without remarkable comorbidities.No association was found between the number of mtDNA variants in genes encoding proteins, tRNAs, rRNAs, and in non-coding regions in the different study groups. Next, variants that controls shared with the other groups were discarded. A significantly higher number of exclusive variants was observed in the D-loop region for the HTG group (~1.23 variants/subject), in contrast to controls (~0.35 variants/subject). In the D-loop, specifically in the 7S DNA sub-region within the Hypervariable region 1 (HV1), we found that 42% of the HTG and 27% of the NTG subjects presented variants, while this was only 14% for the controls and OH subjects. As we have previously reported a reduction in mtDNA copy number in HTG, we analysed if specific D-loop variants could explain this. While the majority of glaucoma patients with the exclusive D-loop variants m.72T>C, m.16163 A>G, m.16186C>T, m.16298T>C, and m.16390G>A presented a mtDNA copy number below controls median, no significant association between these variants and low copy number was found and their possible negative role in mtDNA replication remains uncertain. Approximately 38% of the HTG patients with reduced copy number did not carry any exclusive D-loop or other mtDNA variants, which indicates that variants in nuclear-encoded mitochondrial genes, environmental factors, or aging might be involved in those cases.In conclusion, we found that variants in the D-loop region may be a risk factor in a subgroup of POAG, possibly by affecting mtDNA replication.
原发性开角型青光眼（POAG）是一种特征性视神经病变，由视神经形成神经元--视网膜神经节细胞（RGC）变性引起。高眼压（IOP）和衰老已被确定为主要的风险因素；然而，POAG 的病理生理学尚不完全清楚。由于 RGC 需要大量能量，线粒体功能障碍可能会危及 RGC 的存活。我们在水衣 DNA 中探讨了 mtDNA 变异及其在整个 mtDNA 中的分布是否可能成为 POAG 的风险因素。我们对年龄和性别匹配的研究群体进行了 mtDNA 测序，这些群体包括高度紧张性青光眼（HTG，71 人）、正常紧张性青光眼患者（NTG，33 人）、眼部高血压受试者（OH，7 人）和白内障对照组（无青光眼，30 人），他们都没有明显的合并症。在不同研究组中，编码蛋白质、tRNA、rRNA 的基因和非编码区中的 mtDNA 变异数量之间没有发现关联。接下来，我们剔除了与其他研究组共享的控制变异。与对照组（约 0.35 个变体/受试者）相比，HTG 组（约 1.23 个变体/受试者）在 D 环区域观察到的排他性变体数量明显较高。我们发现，在 D 环，特别是在超变异区 1（HV1）内的 7S DNA 亚区，42%的 HTG 受试者和 27% 的 NTG 受试者出现了变异，而对照组和 OH 受试者只有 14%出现变异。由于我们以前曾报道过 HTG 中 mtDNA 拷贝数的减少，因此我们分析了特定的 D 环变异是否能解释这一现象。虽然大部分青光眼患者的 m.72T>C、m.16163 A>G、m.16186C>T、m.16298T>C 和 m.16390G>A 等专属 D 环变异的 mtDNA 拷贝数低于对照组的中位数，但并没有发现这些变异与低拷贝数之间存在显著关联，它们在 mtDNA 复制中可能起到的负面作用仍不确定。在拷贝数降低的 HTG 患者中，约有 38% 不携带任何 D 环或其他 mtDNA 变异，这表明这些病例可能与核编码线粒体基因的变异、环境因素或衰老有关。
{"title":"Mitochondrial DNA D-loop variants correlate with a primary open-angle glaucoma subgroup","authors":"A. Vallbona-Garcia, Patrick J. Lindsey, Rick Kamps, A. Stassen, Nhan Nguyen, F. van Tienen, Ilse H. J. Hamers, Rianne Hardij, Marike W. van Gisbergen, Birke J. Benedikter, Irenaeus F. M. de Coo, C. A. Webers, Theo G. M. F. Gorgels, H. J. Smeets","doi":"10.3389/fopht.2023.1309836","DOIUrl":"https://doi.org/10.3389/fopht.2023.1309836","url":null,"abstract":"Primary open-angle glaucoma (POAG) is a characteristic optic neuropathy, caused by degeneration of the optic nerve-forming neurons, the retinal ganglion cells (RGCs). High intraocular pressure (IOP) and aging have been identified as major risk factors; yet the POAG pathophysiology is not fully understood. Since RGCs have high energy requirements, mitochondrial dysfunction may put the survivability of RGCs at risk. We explored in buffy coat DNA whether mtDNA variants and their distribution throughout the mtDNA could be risk factors for POAG.The mtDNA was sequenced from age- and sex-matched study groups, being high tension glaucoma (HTG, n=71), normal tension glaucoma patients (NTG, n=33), ocular hypertensive subjects (OH, n=7), and cataract controls (without glaucoma; n=30), all without remarkable comorbidities.No association was found between the number of mtDNA variants in genes encoding proteins, tRNAs, rRNAs, and in non-coding regions in the different study groups. Next, variants that controls shared with the other groups were discarded. A significantly higher number of exclusive variants was observed in the D-loop region for the HTG group (~1.23 variants/subject), in contrast to controls (~0.35 variants/subject). In the D-loop, specifically in the 7S DNA sub-region within the Hypervariable region 1 (HV1), we found that 42% of the HTG and 27% of the NTG subjects presented variants, while this was only 14% for the controls and OH subjects. As we have previously reported a reduction in mtDNA copy number in HTG, we analysed if specific D-loop variants could explain this. While the majority of glaucoma patients with the exclusive D-loop variants m.72T>C, m.16163 A>G, m.16186C>T, m.16298T>C, and m.16390G>A presented a mtDNA copy number below controls median, no significant association between these variants and low copy number was found and their possible negative role in mtDNA replication remains uncertain. Approximately 38% of the HTG patients with reduced copy number did not carry any exclusive D-loop or other mtDNA variants, which indicates that variants in nuclear-encoded mitochondrial genes, environmental factors, or aging might be involved in those cases.In conclusion, we found that variants in the D-loop region may be a risk factor in a subgroup of POAG, possibly by affecting mtDNA replication.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"59 40","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139527239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-15DOI: 10.3389/fopht.2023.1334602
Chunxu Yuan, L. Gerhards, I. Solov’yov, Karin Dedek
Gap junctions transmit electrical signals in neurons and serve metabolic coupling and chemical communication. Gap junctions are made of intercellular channels with large pores, allowing ions and small molecules to permeate. In the mammalian retina, intercellular coupling fulfills many vital functions in visual signal processing but is also implicated in promoting cell death after insults, such as excitotoxicity or hypoxia. Conversely, some studies also suggested a role for retinal gap junctions in neuroprotection. Recently, gap junctions were also advocated as conduits for therapeutic drug delivery in neurodegenerative disorders. This requires the permeation of rather large molecules through retinal gap junctions. However, the permeability of retinal networks for molecules >0.6 kDa has not been tested systematically. Here, we used the cut-loading method and probed gap junctional networks in the mouse retina for their permeability to cGMP and cAMP coupled to Biotin, using the well-characterized tracer Neurobiotin as control. Biotin-cGMP and -cAMP have a molecular weight of >0.8 kDa. We show that they cannot pass the gap junctions of horizontal cells but can permeate through the gap junctions of specific amacrine cells in the inner retina. These amacrine cells do not comprise AII amacrine cells and nitric oxide-releasing amacrine cells but some unknown type. In summary, we show that some retinal gap junctions are large enough to let molecules >0.8 kDa pass, making the intercellular delivery of therapeutic agents – already successfully exploited, for example, in cancer – also feasible in neurodegenerative diseases.
{"title":"Biotin-cGMP and -cAMP are able to permeate through the gap junctions of some amacrine cells in the mouse retina despite their large size","authors":"Chunxu Yuan, L. Gerhards, I. Solov’yov, Karin Dedek","doi":"10.3389/fopht.2023.1334602","DOIUrl":"https://doi.org/10.3389/fopht.2023.1334602","url":null,"abstract":"Gap junctions transmit electrical signals in neurons and serve metabolic coupling and chemical communication. Gap junctions are made of intercellular channels with large pores, allowing ions and small molecules to permeate. In the mammalian retina, intercellular coupling fulfills many vital functions in visual signal processing but is also implicated in promoting cell death after insults, such as excitotoxicity or hypoxia. Conversely, some studies also suggested a role for retinal gap junctions in neuroprotection. Recently, gap junctions were also advocated as conduits for therapeutic drug delivery in neurodegenerative disorders. This requires the permeation of rather large molecules through retinal gap junctions. However, the permeability of retinal networks for molecules >0.6 kDa has not been tested systematically. Here, we used the cut-loading method and probed gap junctional networks in the mouse retina for their permeability to cGMP and cAMP coupled to Biotin, using the well-characterized tracer Neurobiotin as control. Biotin-cGMP and -cAMP have a molecular weight of >0.8 kDa. We show that they cannot pass the gap junctions of horizontal cells but can permeate through the gap junctions of specific amacrine cells in the inner retina. These amacrine cells do not comprise AII amacrine cells and nitric oxide-releasing amacrine cells but some unknown type. In summary, we show that some retinal gap junctions are large enough to let molecules >0.8 kDa pass, making the intercellular delivery of therapeutic agents – already successfully exploited, for example, in cancer – also feasible in neurodegenerative diseases.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"31 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139529284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-10DOI: 10.3389/fopht.2023.1303723
Tais Estrela, L. Dagi
Craniosynostosis (CS) or the premature fusion of one or more cranial sutures in utero, or during the first years of life, can present in isolation or as a multisystem clinical disorder with a particular impact on visual function. Among ophthalmic complications, optic neuropathy is a significant cause of irreversible vision loss in these patients. Children with CS are at higher risk of developing elevated intracranial pressure which can lead to papilledema and, ultimately, optic atrophy. In addition, sometimes associated obstructive sleep apnea, abnormalities in central nervous system venous development, and Chiari malformation may contribute to optic neuropathy. Ophthalmologists have an important role in managing a number of coexistent ophthalmologic complications such as strabismus, anisometropia, amblyopia, ptosis, and exposure keratopathy in addition to maintaining surveillance for early signs of optic neuropathy; they play a critical consultative role contributing to the decision for primary or repeat decompressive surgery. In this article, we aim to review the etiology, diagnostic approach, and management of optic neuropathies in patients with craniosynostosis.
{"title":"Optic neuropathy in craniosynostosis","authors":"Tais Estrela, L. Dagi","doi":"10.3389/fopht.2023.1303723","DOIUrl":"https://doi.org/10.3389/fopht.2023.1303723","url":null,"abstract":"Craniosynostosis (CS) or the premature fusion of one or more cranial sutures in utero, or during the first years of life, can present in isolation or as a multisystem clinical disorder with a particular impact on visual function. Among ophthalmic complications, optic neuropathy is a significant cause of irreversible vision loss in these patients. Children with CS are at higher risk of developing elevated intracranial pressure which can lead to papilledema and, ultimately, optic atrophy. In addition, sometimes associated obstructive sleep apnea, abnormalities in central nervous system venous development, and Chiari malformation may contribute to optic neuropathy. Ophthalmologists have an important role in managing a number of coexistent ophthalmologic complications such as strabismus, anisometropia, amblyopia, ptosis, and exposure keratopathy in addition to maintaining surveillance for early signs of optic neuropathy; they play a critical consultative role contributing to the decision for primary or repeat decompressive surgery. In this article, we aim to review the etiology, diagnostic approach, and management of optic neuropathies in patients with craniosynostosis.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"11 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139439799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-08DOI: 10.3389/fopht.2023.1310226
Youichi Shinozaki, K. Namekata, Xiaoli Guo, T. Harada
Glial cells, a type of non-neuronal cell found in the central nervous system (CNS), play a critical role in maintaining homeostasis and regulating CNS functions. Recent advancements in technology have paved the way for new therapeutic strategies in the fight against glaucoma. While intraocular pressure (IOP) is the most well-known modifiable risk factor, a significant number of glaucoma patients have normal IOP levels. Because glaucoma is a complex, multifactorial disease influenced by various factors that contribute to its onset and progression, it is imperative that we consider factors beyond IOP to effectively prevent or slow down the disease’s advancement. In the realm of CNS neurodegenerative diseases, glial cells have emerged as key players due to their pivotal roles in initiating and hastening disease progression. The inhibition of dysregulated glial function holds the potential to protect neurons and restore brain function. Consequently, glial cells represent an enticing therapeutic candidate for glaucoma, even though the majority of glaucoma research has historically concentrated solely on retinal ganglion cells (RGCs). In addition to the neuroprotection of RGCs, the proper regulation of glial cell function can also facilitate structural and functional recovery in the retina. In this review, we offer an overview of recent advancements in understanding the non-cell-autonomous mechanisms underlying the pathogenesis of glaucoma. Furthermore, state-of-the-art technologies have opened up possibilities for regenerating the optic nerve, which was previously believed to be incapable of regeneration. We will also delve into the potential roles of glial cells in the regeneration of the optic nerve and the restoration of visual function.
{"title":"Glial cells as a promising therapeutic target of glaucoma: beyond the IOP","authors":"Youichi Shinozaki, K. Namekata, Xiaoli Guo, T. Harada","doi":"10.3389/fopht.2023.1310226","DOIUrl":"https://doi.org/10.3389/fopht.2023.1310226","url":null,"abstract":"Glial cells, a type of non-neuronal cell found in the central nervous system (CNS), play a critical role in maintaining homeostasis and regulating CNS functions. Recent advancements in technology have paved the way for new therapeutic strategies in the fight against glaucoma. While intraocular pressure (IOP) is the most well-known modifiable risk factor, a significant number of glaucoma patients have normal IOP levels. Because glaucoma is a complex, multifactorial disease influenced by various factors that contribute to its onset and progression, it is imperative that we consider factors beyond IOP to effectively prevent or slow down the disease’s advancement. In the realm of CNS neurodegenerative diseases, glial cells have emerged as key players due to their pivotal roles in initiating and hastening disease progression. The inhibition of dysregulated glial function holds the potential to protect neurons and restore brain function. Consequently, glial cells represent an enticing therapeutic candidate for glaucoma, even though the majority of glaucoma research has historically concentrated solely on retinal ganglion cells (RGCs). In addition to the neuroprotection of RGCs, the proper regulation of glial cell function can also facilitate structural and functional recovery in the retina. In this review, we offer an overview of recent advancements in understanding the non-cell-autonomous mechanisms underlying the pathogenesis of glaucoma. Furthermore, state-of-the-art technologies have opened up possibilities for regenerating the optic nerve, which was previously believed to be incapable of regeneration. We will also delve into the potential roles of glial cells in the regeneration of the optic nerve and the restoration of visual function.","PeriodicalId":510339,"journal":{"name":"Frontiers in Ophthalmology","volume":"59 24","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139447663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：