Publications by authors named "Taimu Sato"
Corrigendum: Glaucoma and microglia-induced neuroinflammation.
Front Ophthalmol (Lausanne)
December 2023
[This corrects the article DOI: 10.3389/fopht.2023.
View Article and Find Full Text PDFArticle Synopsis
- Resident microglia in the central nervous system (CNS), including the retina, play a crucial role in maintaining homeostasis, but their activation during pathological conditions is not well understood.
- This study utilized FACS and RNA-seq to analyze microglial gene expression changes during retinal ganglion cell (RGC) degeneration caused by optic nerve injury, identifying strong expression of neurotoxic factors Tnf and Il1α.
- The findings suggest that targeting Rho kinase and GPR84 signaling pathways could be potential therapeutic strategies to prevent the harmful effects of activated microglia in conditions like traumatic optic neuropathy and glaucoma.
Glaucoma is a multifactorial neurodegenerative disease characterized by a progressive optic neuropathy resulting in visual field defects. Elevated intraocular pressure (IOP) is the greatest risk factor for the development of glaucoma, and IOP reduction therapy is the only treatment currently available. However, there are many cases in which retinal degeneration progresses despite sufficient control of IOP.
View Article and Find Full Text PDFGlaucoma is a leading cause of blindness worldwide and is characterized by degeneration associated with the death of retinal ganglion cells (RGCs). It is believed that glaucoma is a group of heterogeneous diseases with multifactorial pathomechanisms. Here, we investigate whether anti-inflammation treatment with an ER stress blockade can selectively promote neuroprotection against NMDA injury in the RGCs.
View Article and Find Full Text PDFPurpose: To screen for anti-recoverin antibodies in elderly patients with retinitis pigmentosa (RP) with or without cancer and cross-sectionally characterize the seropositive patients clinically.
Methods: Serum from 75 RP patients who had been tested for mutations in a panel of 83 RP genes and 73 normal controls, all aged 50-80 years, were screened for anti-recoverin antibodies by Western blot using recombinant recoverin, retinal lysate from a marmoset and commercial anti-recoverin antibodies as a control.
Results: Three RP patients with typical pigmentary degeneration of the 75 (4.