Kyushu University Academic Staff Educational and Research Activities Database
List of Reports
Yusuke Murakami Last modified date:2023.12.08

Lecturer / Ophthalmology / Kyushu University Hospital


Reports
1. Jonathan B Lin, Yusuke Murakami, Joan W Miller, Demetrios G Vavvas, Neuroprotection for Age-Related Macular Degeneration., Ophthalmology science, 10.1016/j.xops.2022.100192, Vol.2, No.4, p.100192, 2022.12, Age-related macular degeneration (AMD) is a leading cause of blindness worldwide. Early to intermediate AMD is characterized by the accumulation of lipid- and protein-rich drusen. Late stages of the disease are characterized by the development of choroidal neovascularization, termed "exudative" or "neovascular AMD," or retinal pigment epithelium (RPE) cell and photoreceptor death, termed "geographic atrophy" (GA) in advanced nonexudative AMD. Although we have effective treatments for exudative AMD in the form of anti-VEGF agents, they have no role for patients with GA. Neuroprotection strategies have emerged as a possible way to slow photoreceptor degeneration and vision loss in patients with GA. These approaches include reduction of oxidative stress, modulation of the visual cycle, reduction of toxic molecules, inhibition of pathologic protein activity, prevention of cellular apoptosis or programmed necrosis (necroptosis), inhibition of inflammation, direct activation of neurotrophic factors, delivery of umbilical tissue-derived cells, and RPE replacement. Despite active investigation in this area and significant promise based on preclinical studies, many clinical studies have not yielded successful results. We discuss selected past and current neuroprotection trials for AMD, highlight the lessons learned from these past studies, and discuss our perspective regarding remaining questions that must be answered before neuroprotection can be successfully applied in the field of AMD research..
2. Yan Tao, Yusuke Murakami, Demetrios G Vavvas, Koh-Hei Sonoda, Necroptosis and Neuroinflammation in Retinal Degeneration., Frontiers in neuroscience, 10.3389/fnins.2022.911430, Vol.16, p.911430, 2022.06, Necroptosis mediates the chronic inflammatory phenotype in neurodegeneration. Receptor-interacting protein kinase (RIPK) plays a pivotal role in the induction of necroptosis in various cell types, including microglia, and it is implicated in diverse neurodegenerative diseases in the central nervous system and the retina. Targeting RIPK has been proven beneficial for alleviating both neuroinflammation and degeneration in basic/preclinical studies. In this review, we discuss the role of necroptosis in retinal degeneration, including (1) the molecular pathways involving RIPK, (2) RIPK-dependent microglial activation and necroptosis, and (3) the interactions between necroptosis and retinal neuroinflammation/degeneration. This review will contribute to a renewed focus on neuroinflammation induced by necroptosis and to the development of anti-RIPK drugs against retinal degeneration..
3. Murakami Y, Nakabeppu Y, Sonoda KH, Oxidative Stress and Microglial Response in Retinitis Pigmentosa, 2020.09.
4. Takeda A, Yanai R, Murakami Y, Arima M, Sonoda KH, New insights into immunological therapy for retinal disorders, Frontiers in immunology, 10.3389/fimmu.2020.01431, Vol.11, p.1431, 2020.07, In the twentieth century, a conspicuous lack of effective treatment strategies existed for managing several retinal disorders, including age-related macular degeneration; diabetic retinopathy (DR); retinopathy of prematurity (ROP); retinitis pigmentosa (RP); uveitis, including Behçet's disease; and vitreoretinal lymphoma (VRL). However, in the first decade of this century, advances in biomedicine have provided new treatment strategies in the field of ophthalmology, particularly biologics that target vascular endothelial growth factor or tumor necrosis factor (TNF)-α. Furthermore, clinical trials on gene therapy specifically for patients with autosomal recessive or X-linked RP have commenced. The overall survival rates of patients with VRL have improved, owing to earlier diagnoses and better treatment strategies. However, some unresolved problems remain such as primary or secondary non-response to biologics or chemotherapy, and the lack of adequate strategies for treating most RP patients. In this review, we provide an overview of the immunological mechanisms of the eye under normal conditions and in several retinal disorders, including uveitis, DR, ROP, RP, and VRL. In addition, we discuss recent studies that describe the inflammatory responses that occur during the course of these retinal disorders to provide new insights into their diagnosis and treatment..
5. Murakami Y, Nakao S, Ishikawa K, Sonoda KH, Innate immune response in retinal homeostasis and inflammatory disorders, Progress in retinal and eye research, 10.1016/j.preteyeres.2019.100778, Vol.74, p.100778, 2020.01, Innate immune cells such as neutrophils, monocyte-macrophages and microglial cells are pivotal for the health and disease of the retina. For the maintenance of retinal homeostasis, these cells and immunosuppressive molecules in the eye actively regulate the induction and the expression of inflammation in order to prevent excessive activation and subsequent tissue damage. In the disease context, these regulatory mechanisms are modulated genetically and/or by environmental stimuli such as damage-associated molecular patterns (DAMPs), and a chronic innate immune response regulates or contributes to the formation of diverse retinal disorders such as uveitis, retinitis pigmentosa, retinal vascular diseases and retinal fibrosis. Here we summarize the recent knowledge regarding the innate immune response in both ocular immune regulation and inflammatory retinal diseases, and we describe the potential of the innate immune response as a biomarker and therapeutic target..
6. Necrotic cone photoreceptor cell death in retinitis pigmentosa.
7. Photoreceptor cell death and rescue in retinal detachment and degenerations
Photoreceptor cell death is the ultimate cause of vision loss in various retinal disorders, including retinal detachment (RD). Photoreceptor cell death has been thought to occur mainly through apoptosis, which is the most characterized form of programmed cell death. The caspase family of cysteine proteases plays a central role for inducing apoptosis, and in experimental models of RD, dying photoreceptor cells exhibit caspase activation; however, there is a paradox that caspase inhibition alone does not provide a sufficient protection against photoreceptor cell loss, suggesting that other mechanisms of cell death are involved. Recent accumulating evidence demonstrates that non-apoptotic forms of cell death, such as autophagy and necrosis, are also regulated by specific molecular machinery, such as those mediated by autophagy-related proteins and receptor-interacting protein kinases, respectively. Here we summarize the current knowledge of cell death signaling and its roles in photoreceptor cell death after RD and other retinal degenerative diseases. A body of studies indicate that not only apoptotic but also autophagic and necrotic signaling are involved in photoreceptor cell death, and that combined targeting of these pathways may be an effective neuroprotective strategy for retinal diseases associated with photoreceptor cell loss..
8. Comprehensive Strategy for Retinal Neuroprotection : Challenging the Clinical Application.
9. Mitsuho Onimaru, Yoshikazu Yonemitsu, Yusuke Murakami, Yasuhiro Ikeda, Katsuo Sueishi, PKC-MMP-14 Axis Regulates Endothelial Soluble Tie-2 (sTie-2) Production: Involvement of sTie-2 in Diabetes Mellitus-Associated Vascular Complications, CIRCULATION, Vol.124, No.21, 2011.11.
10. Prospect of novel therapeutic approaches to treatment of retinitis pigmentosa: gene therapy and retinal prosthesis.