Publications by authors named "U Jurkunas"
Purpose: To investigate the effectiveness of mitochondrial-targeted antioxidant mitoquinone (MitoQ) and nontargeted antioxidant idebenone (Idb) in alleviating mitochondrial dysfunction in corneal endothelial cells (CEnCs).
Methods: In vitro experiments were conducted using immortalized normal human corneal endothelial cells (HCEnC-21T; SVN1-67F) and Fuchs endothelial corneal dystrophy (FECD) cells (SVF5-54F; SVF3-76M). Cells were pretreated with MitoQ or Idb and then exposed to menadione (MN) with simultaneous antioxidant treatment.
Article Synopsis
- The study aimed to explore the relationship between limbal stem cell deficiency (LSCD) and neurotrophic keratopathy in patients with ocular graft-vs-host disease (oGVHD).
- Medical records from 28 oGVHD patients were analyzed, revealing that 50% had partial LSCD and 32% had complete LSCD, with significant differences in nerve density and corneal sensitivity between groups.
- The findings suggest a strong connection between LSCD, neurodegeneration, and inflammation in oGVHD patients.
Fuchs Endothelial Corneal Dystrophy (FECD) is an aging disorder characterized by expedited loss of corneal endothelial cells (CEnCs) and heightened DNA damage compared to normal CEnCs. We previously established that ultraviolet-A (UVA) light causes DNA damage and leads to FECD phenotype in a non-genetic mouse model. Here, we demonstrate that acute treatment with chemical stressor, menadione, or physiological stressors, UVA, and catechol estrogen (4-OHE), results in an early and increased activation of ATM-mediated DNA damage response in FECD compared to normal CEnCs.
View Article and Find Full Text PDFThank you for your thoughtful and insightful commentary on our paper, "Outcomes of Boston Keratoprosthesis Type I Implantation in Poland: A Retrospective Study on 118 Patients" [...
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- Epidemiological studies indicate that cigarette smoking worsens corneal endothelial dysfunction, but the exact reasons are not well understood.
- The research found that prolonged exposure to smoke activates the aryl hydrocarbon receptor (AhR), which increases the expression of CYP1B1 and leads to aging and scarring in corneal cells, possibly as a way to adapt to damage.
- While these changes suggest early signs of dysfunction, no severe damage was detected, implying that developing a serious condition like Fuchs endothelial corneal dystrophy requires other environmental or genetic influences beyond just smoking.