Nagoya University · Medicine
Professor Hiroki Kaneko's research lab focuses on retinal diseases, particularly the molecular and cellular mechanisms underlying retinal degeneration in conditions such as diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration. The lab investigates the roles of oxidative stress, inflammation, neurotrophic factors like BDNF, and microRNAs in retinal cell damage and repair. A key focus is on the pathogenesis of retinal pigment epithelial (RPE) cell dysfunction, including epithelial-mesenchymal transition (EMT) and oxidative injury induced by environmental stressors such as blue light and high glucose. The lab also explores protective pathways, such as the Nrf2 antioxidant system, and the therapeutic potential of n-3 fatty acids and neurotrophic factors.
Figures are computed from collected data and may differ slightly.
In response to retinal damage, numerous BM-derived cells migrated to the retina from the ciliary body, optic nerve, and retinal vessels and differentiated into microglia. The higher rate of immunologic activation and the increased specificity to the damaged site appeared to be the characteristic features of BM-derived microglia.
Diabetic retinopathy (DR) is a widespread vision-threatening disease, and neuroretinal abnormality should be considered as an important problem. Brain-derived neurotrophic factor (BDNF) has recently been considered as a possible treatment to prevent DR-induced neuroretinal damage, but how BDNF is upregulated in DR remains unclear. We found an increase in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) in the vitreous of patients with DR. We confirmed that human retinal endothelial cells secreted
Oxidative stress and inflammation play crucial roles in the development and progression of retinal diseases. Retinal damage by various etiologies can result in retinopathy of prematurity (ROP), diabetic retinopathy (DR), and age-related macular degeneration (AMD). n-3 fatty acids are essential fatty acids and are necessary for homeostasis. They are important retinal membrane components and are involved in energy storage. n-3 fatty acids also have antioxidant and anti-inflammatory properties, and
The results of the present study indicate that hsa-miR-148a-3p was specifically detected in RD and promotes EMT in RPE.
Even with a high surgical success rate for retinal detachment and proliferative vitreoretinopathy (PVR) supported by the robust improvement in vitrectomy surgery and its related devices, certain questions still remain for the pathogenesis and treatment of PVR. One of the important biological events in PVR is epithelial-mesenchymal transition (EMT) of the retinal pigment epithelial (RPE) cells. MicroRNAs are noncoding, small, single-strand RNAs that posttranscriptionally regulate gene expression
<i>Purpose</i>. It is a matter of increasing concern that exposure to light-emitting diodes (LED), particularly blue light (BL), damages retinal cells. This study aimed to investigate the retinal pigment epithelium (RPE) damage caused by BL and to elucidate the role of nuclear factor (erythroid-derived)-related factor 2 (Nrf2) in the pathogenesis of BL-induced RPE damage. <i>Methods</i>. ARPE-19, a human RPE cell line, and mouse primary RPE cells from wild-type and <i>Nrf2</i> knockout (<i>Nrf2<
Silicone oil (SO) is an intraocular surgical adjuvant that reduces the surgical complications in refractory retinal diseases, although membrane and cellular proliferation is often seen even in SO-filled eyes. We hypothesised that the fluid in the space between the SO and the retina, named the "sub-silicone oil fluid (SOF)", enhances these biological responses. We proposed a safe method for SOF extraction. We also analysed inflammatory cytokine expressions and SOF osmotic pressures from eyes with
These results indicated that Caveolin-1 in RPE cells prevents PVR by blocking EMT.
Enhanced expression of caveolin-1 successfully blocked epithelial-mesenchymal transition of RPE and the reduction of subretinal fibrosis in mice. Nevertheless, in exchange for blocking subretinal fibrosis, caveolin-1 promotes RPE cellular senescence and might affect the progression of geographic atrophy in AMD.
H4 receptors are expressed in macrophages that accumulate around CNVs. Suppressing H4 receptor expression prevented the pathological vessel leakage without showing retinal toxicity, indicating that the H4 receptor has potential as a novel therapeutic target in AMD.
Polypoidal choroidal vasculopathy (PCV) is characterized by polyp-like choroidal neovascularization and a branching vascular network. Intravitreal aflibercept injection (IAI) or photodynamic therapy (PDT) is used for treatment. We retrospectively compared the 1-year outcomes of IAI monotherapy and its combination with initial PDT for PCV. Twelve eyes with naïve PCV received three IAIs and a single PDT after the first IAI and as needed injection (combination group); 11 eyes with naïve PCV receive
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