Key Takeaways

  • Researchers discovered how abnormal collagen excrescences, or guttata, on the Descemet membrane contribute to Fuchs endothelial corneal dystrophy (FECD), a leading cause of corneal blindness.
  • Study findings suggest that guttata-like structures induce human corneal endothelial cell loss, with FECD-derived cells more sensitive to this stress compared with normal cells.
  • These findings could pave the way for alternative treatment strategies for FECD and potentially reduce the need for corneal transplants in some patients.

Researchers from the University of Waterloo have discovered how physical microstructures on the Descemet membrane contribute to Fuchs endothelial corneal dystrophy (FECD), a leading cause of corneal blindness and corneal transplantation worldwide. With donated corneas in short global supply, the finding could lead to alternative treatment strategies and reduce the need for corneal transplants in some patients.

“Our ultimate goal is the development of alternative treatments, which could mean fewer people will need transplants for corneal blindness due to Fuchs endothelial corneal dystrophy in the future,” said Evelyn Yim, PhD, PEng, a chemical engineering professor at Waterloo and the Canada Research Chair in Nanomaterials for Regenerative Medicine.

FECD is characterized by human corneal endothelial cell (HCEC) loss, which causes the cornea to become cloudy and leads to impaired vision, and the formation of discrete abnormal collagen excrescences, or guttata, on the Descemet membrane. Scientists have known for years that these microstructures develop in eyes with FECD, but they were thought to be a sign of the disease and not a cause of further damage.

“When the cornea becomes cloudy, the condition is in an advanced stage,” said Lexie Xi, a Waterloo PhD candidate in chemical engineering and first author of the study. “We aim to understand the disease mechanism to develop better alternative treatments.”

Researchers utilized an in vitro synthetic-guttata model to investigate the mechanobiological effect of guttata microtopography on HCEC apoptosis. Study findings suggest that guttata-like structures can induce HCEC apoptosis, and FECD-derived cells are more sensitive to guttata-induced topographical stress compared with normal HCECs. Furthermore, topography-induced apoptosis is mediated by enhanced cytoskeletal contractility.

These findings could help researchers develop new ways to treat FECD by addressing the underlying causes of cell damage. Potential approaches include cell-based therapies to replace damaged cells or procedures to remove guttata that contribute to cell death. Although further research is needed, such strategies could eventually reduce the need for corneal transplants in some patients.

The research team also included Stephan Ong Tone, MDCM, PhD, FRCSC, a corneal surgeon at the Sunnybrook Research Institute in Toronto, and Gary S.L. Peh, BSc, GradDip Reprod Sci, PhD, and Jodhbir S. Mehta, MBBS, FRCOphth, FRCS(Ed), FAMS, PhD, from the Singapore Eye Research Institute.

The study, Corneal guttata-like microtopography induces corneal endothelial cell apoptosis by modulating mechanotransduction, was recently published in Cell Biomaterials.1

  1. Xi LWQ, Enkhbat M, Jain D, et al. Corneal guttata-like microtopography induces corneal endothelial cell apoptosis by modulating mechanotransduction. Cell Biomaterials. 2026; 100510. doi:10.1016/j.celbio.2026.100510