Corneal surgery and disorders

This paper reinterprets keratoconus gene expression by showing that expression direction depends on control choice and stromal state, not disease causation or intervention effectiveness.

This study identifies reduced NEAT1 expression in the central corneal endothelium as a factor increasing susceptibility to oxidative stress in Fuchs Endothelial Corneal Dystrophy.

This study shows ferritinophagy contributes to iron accumulation and ferroptosis in FECD, with UVA exposure activating this process.

This study shows that ferroptosis is linked to guttae formation in a murine model of Fuchs endothelial corneal dystrophy, providing a model for testing ferroptosis-targeted therapies.

This study examines SKC mice to identify corneal phenotypes related to keratoconus, finding lower penetrance and male-specific abnormalities.

This paper investigates TAZ deficiency in a mouse model of FECD, identifying ER stress, mitochondrial dysfunction, and altered ECM organization as key pathogenic mechanisms.

This study combines monogenic and polygenic risk factors to predict disease progression in Fuchs endothelial corneal dystrophy, showing improved prediction when integrating both factors.

This study evaluates EGCG's protective effects against enzymatic stromal degradation in goat and sheep corneas and validates these animals as ex vivo models for keratoconus research.

This study identifies increased MDA and GPX3 in KC tears and NRF2 dysfunction in stromal cells, suggesting potential biomarkers and therapeutic targets for keratoconus.

This study investigates how reduced substrate stiffness affects corneal endothelial cell health, finding increased FAK activity and EndMT, but no improvement in disease progression with FAK inhibition.

This study shows proteasomal dysfunction causes ER stress, endo-mesenchymal transition, oxidative stress, and apoptosis in mice, leading to FECD-like features.

This paper introduces a new corneal cross-linking method using photo-initiators and visible blue light, which is safer and more effective for thin corneas than the standard riboflavin/UVA protocol.

This paper develops a zebrafish model of macular corneal dystrophy by knocking out the chst6 gene, showing age-dependent corneal abnormalities and structural defects.

The paper identifies Tyr as the gene responsible for the Cctq1a QTL and shows that developmental light exposure interacts with genotype to influence central corneal thickness.

The paper identifies up-regulation of the mTORC1 pathway in keratoconus corneas and confirms differential expression of GWAS risk loci.