Furthermore, FoxO3a increased fibrogenic gene expression, which was reversed by FoxO3a knockdown. TGF-β-mediated FoxO3a overexpression in HSCs facilitated hepatic fibrogenesis, suggesting that FoxO3a may be a novel target for liver fibrosis prevention and treatment.
  The purpose of this study was to perform a detailed longitudinal phenotyping of X-linked retinitis pigmentosa (RP) caused by mutations in the RPGR gene during a long follow-up period.
 
  An Italian cohort of 48 male patients (from 31 unrelated families) with RPGR-associated RP was clinically assessed at a single center (mean follow-up = 6.5 years), including measurements of best-corrected visual acuity (BCVA), Goldmann visual field (GVF), optical coherence tomography (OCT), fundus autofluorescence (FAF), microperimetry, and full-field electroretinography (ERG).
 
  Patients (29.6 ± 15.2 years) showed a mean BCVA of 0.6 ± 0.7 logMAR, mostly with myopic refraction (79.2%). Thirty patients (62.5%) presented a typical RP fundus, while the remaining sine pigmento RP. Over the follow-up, BCVA significantly declined at a mean rate of 0.025 logMAR/year. Typical RP and high myopia were associated with a significantly faster decline of BCVA. Blindness was driven primarily by GVF loss. ERG responses with a rod-cone pattern of dysfunction were detectable in patients (50%) that were significantly younger and more frequently presented sine pigmento RP. Thirteen patients (27.1%) had macular abnormalities without cystoid macular edema. Patients (50%) with a perimacular hyper-FAF ring were significantly younger, had a higher BCVA and a better-preserved ellipsoid zone band than those with markedly decreased FAF. Patients harboring pathogenic variants in exons 1 to 14 showed a milder phenotype compared to those with ORF15 mutations.
 
  Our monocentric, longitudinal retrospective study revealed a spectrum disease progression in male patients with RPGR-associated RP. Slow disease progression correlated with sine pigmento RP, absence of high myopia, and mutations in RPGR exons 1 to 14.
 Our monocentric, longitudinal retrospective study revealed a spectrum disease progression in male patients with RPGR-associated RP. Slow disease progression correlated with sine pigmento RP, absence of high myopia, and mutations in RPGR exons 1 to 14.
  Hyperglycemia damages the retinal mitochondria, and the mitochondrial damage plays a central role in the development of diabetic retinopathy. Patients with diabetes also have higher homocysteine levels, and abnormalities in homocysteine metabolism result in decreased levels of hydrogen sulfide (H2S), an endogenous gasotransmitter signaling molecule with antioxidant properties. This study aimed to investigate the role of H2S in the development of diabetic retinopathy.
 
  Streptozotocin-induced diabetic mice were administered a slow releasing H2S donor GYY4137 for 6 months.  https://www.selleckchem.com/products/ly3023414.html  The retina was used to measure H2S levels, and their retinal vasculature was analyzed for the histopathology characteristic of diabetic retinopathy and oxidative stress, mitochondrial damaging matrix metalloproteinase-9 (MMP-9), and mitochondrial integrity. These parameters were also measured in the isolated retinal endothelial cells incubated in high glucose medium containing GYY4137.
 
  Administration of GYY4137 to diabetic mice ameliorated decrease in H2S and prevented the development of histopathology, characteristic of diabetic retinopathy. Diabetes-induced increase in oxidative stress, MMP-9 activation, and mitochondrial damage were also attenuated in mice receiving GYY4137. Results from isolated retinal endothelial cells confirmed the results obtained from diabetic mice.
 
  Thus, supplementation of H2S donor prevents the development of diabetic retinopathy by ameliorating increase in oxidative stress and preserving the mitochondrial integrity. H2S donors may provide a novel therapeutic strategy to inhibit the development of diabetic retinopathy.
 Thus, supplementation of H2S donor prevents the development of diabetic retinopathy by ameliorating increase in oxidative stress and preserving the mitochondrial integrity. H2S donors may provide a novel therapeutic strategy to inhibit the development of diabetic retinopathy.
  Ocular structural and functional changes, collectively termed spaceflight-associated neuro-ocular syndrome (SANS), have been described in astronauts undergoing long-duration missions in the microgravity environment of the International Space Station. We tested the hypothesis that retinal vascular remodeling, particularly by smaller vessels, mediates the chronic headward fluid shifts associated with SANS.
 
  As a retrospective study, arterial and venous patterns extracted from 30° infrared Heidelberg Spectralis retinal images of eight crew members acquired before and after six-month missions were analyzed with NASA's recently released VESsel GENeration Analysis (VESGEN) software. Output parameters included the fractal dimension and overall vessel length density that was further classified into large and small vascular branching generations. Vascular results were compared with SANS-associated clinical ocular measures.
 
  Significant postflight decreases in Df, Lv, and in smaller but not larger vessels were quanher research is required to better characterize retinal microvascular adaptations.
  To evaluate the focal structure-function associations among visual field (VF) loss, optical coherence tomography angiography (OCT-A) vascular measurements, and optical coherence tomography (OCT) structural measurements in glaucoma.
 
  In this cross-sectional study, subjects underwent standard automated perimetry, OCT-based nerve fiber thickness measurements, and OCT-A imaging. Mappings of focal VF test locations with OCT and OCT-A measurements were defined using anatomically adjusted nerve fiber trajectories and were studied using multivariate mixed-effects analysis. Segmented regression analysis was used to determine the presence of breakpoints in the structure-function associations.
 
  The study included 119 eyes from 86 Chinese subjects with primary open-angle glaucoma (POAG). VF mean deviation was significantly associated with global capillary perfusion density (β = 0.13 ± 0.08) and global retinal nerve fiber layer thickness (β = 0.09 ± 0.02). Focal capillary density (FCD) was significantly associated with VF losses at 34 VF test locations (66.