Cultured human corneal endothelial cell-based therapy for treatment of Fuchs endothelial corneal dystrophy
Editorial Commentary

Cultured human corneal endothelial cell-based therapy for treatment of Fuchs endothelial corneal dystrophy

Deepika Malhotra1 ORCID logo, Jodhbir S. Mehta1,2,3,4,5,6,7,8,9

1Cornea and Refractive Service, Singapore National Eye Centre, Singapore, Singapore; 2Clinical Innovation in Ophthalmology, Singapore National Eye Centre, Singapore, Singapore; 3Singapore Eye Research Institute (SERI), Singapore, Singapore; 4Centre of Vision Research, Duke-NUS, Singapore, Singapore; 5Ophthalmology and Visual Sciences Academic Clinical Programme, SingHealth Duke-NUS Academic Medical Centre (AMC), Singapore, Singapore; 6Duke-NUS Graduate Medical School, Singapore, Singapore; 7Yong Loo Lin School of Medicine, Department of Ophthalmology, National University of Singapore, Singapore, Singapore; 8Singhealth-Duke Cell Therapy Centre, Singapore, Singapore; 9Singhealth Transplant Centre, Singapore, Singapore

Correspondence to: Jodhbir S. Mehta, Hons, MBBS, PhD, FRCOphth, FRCS (Ed), FAMS, FARVO. Cornea and Refractive Service, Singapore National Eye Centre, 11 Third Hospital Avenue, #08-00, Singapore 168751, Singapore; Clinical Innovation in Ophthalmology, Singapore National Eye Centre, Singapore, Singapore; Singapore Eye Research Institute (SERI), Singapore, Singapore; Centre of Vision Research, Duke-NUS, Singapore, Singapore; Ophthalmology and Visual Sciences Academic Clinical Programme, SingHealth Duke-NUS Academic Medical Centre (AMC), Singapore, Singapore; Duke-NUS Graduate Medical School, Singapore, Singapore; Yong Loo Lin School of Medicine, Department of Ophthalmology, National University of Singapore, Singapore, Singapore; Singhealth-Duke Cell Therapy Centre, Singapore, Singapore; Singhealth Transplant Centre, Singapore, Singapore. Email: Jodmehta@gmail.com.

Comment on: Tomioka Y, Ueno M, Yamamoto A, et al. Guttae morphology after cultured corneal endothelial cell transplant in Fuchs endothelial corneal dystrophy. JAMA Ophthalmol 2024;142:818-26.


Keywords: Guttae morphology; cell injection therapy; Fuchs endothelial corneal dystrophy (FECD); corneal endothelial cells (CECs)


Received: 26 December 2024; Accepted: 19 June 2025; Published online: 30 June 2025.

doi: 10.21037/aes-24-41


Introduction

Fuchs endothelial corneal dystrophy (FECD) is an inherited, degenerative disease of the corneal endothelial cells (CECs). It is characterized by a progressive deterioration of endothelial cells, altered extracellular matrix (ECM) production, and development of guttae (1,2). The presence of guttae has been shown to significantly impair corneal endothelial function, leading to corneal oedema and visual impairment.

In the last two decades, endothelial keratoplasty has evolved into the mainstay of treatment for endothelial dystrophy, thus largely replacing penetrating keratoplasty (3). However, because of the worldwide shortage of donor corneal tissue, the number of patients needing transplants far exceeds the available donor tissue. A global study published in 2016, focusing on corneal tissue availability, revealed a significant imbalance between supply and demand for corneal transplants. The survey indicated that for every single donor cornea available, there are approximately 70 eyes in need for transplantation (4).

When compared to penetrating keratoplasty, endothelial keratoplasty is associated with better visual outcomes, lower risks of graft rejection, and better long-term survival rates (3,5). Despite recent advancements in surgical methodologies, allogenic grafts continue to be associated with potential long-term risks of failure and rejection. As a result of these challenges related to graft dependency and long-term complications, considerable efforts have been directed over the past decade, towards developing new and alternative therapeutics for FECD. In recent years, there have been a few promising trials of new treatment modalities, which include: regenerative medicine, bioengineered corneal grafts, pharmacological adjuncts, cell-injection therapy, and gene therapy (6-9).

Cell-based treatments entail cultivation of primary human CECs in vitro, using cells obtained from cadaveric donor corneas (10,11). By propagating functional CECs, it is possible to scale up production of these cells from a single donor cornea, providing enough CECs to treat multiple patients. Cultured cells from a single donor can be manufactured to produce treatment for 50–100 recipient eyes (12).

The innovative cell therapy offers enhancements over existing treatment, by streamlining the process and eliminating potential complications such as graft rejection, detachment, dislocation, and graft failure (5).


Abnormal ECM and corneal guttata in FECD

The pathogenesis of FECD entails oxidative stress, altered mitochondrial bioenergetics, and channelopathies resulting in excessive apoptosis and an accelerated loss of CECs (13). Concurrent to endothelial cells loss, the dysfunctional endothelial cells secrete collagen fibrils and basement membrane-like material. This increase in deposition of abnormal ECM at the level of the Descemet’s membrane (DM) forms the warty protuberances or guttae, which is a characteristic finding in FECD (14).

Guttae correlates with the abnormal thickening of the DM and can also become embedded in the thickened membrane, projecting as buried guttae (15). There is an increase in expression of abnormal ECM components leading to excessive deposition of collagens forming abnormal posterior banded and fibrillar layers (16). In the early stages of FECD, guttae are found to be more central and non-confluent. With progressive loss of the endothelial cells, the remaining cells compensate to maintain the monolayer by undergoing pleomorphism and polymegathism. With progression of the disease, there is an increase in both the number and size of guttae. As a result, the endothelial layer is eventually no longer able to maintain the relative corneal dehydration, leading to corneal edema and decompensation with eventual decrease in visual acuity (17).

An in vitro topographical model has shown that increased size and density of guttae, as seen in late-stage FECD, may hinder the reformation of cultured human CEC monolayer after corneal cell injection (18). The results showed that when primary human CECs were injected on top of densely packed synthetic guttata pillars or large diameter pillars of any height and spacing, a corneal endothelial monolayer failed to form. This indicates that guttae could disrupt the migration of injected cells, thereby hampering monolayer formation. Consequently, surgically removing the guttae before cell injection therapy or pharmacotherapy could potentially increase the chance of successful cell therapy in advanced cases of FECD with extensive guttae.

Another study, consistent with the results of Rizwan et al. (18), showed that the diameter of the guttae plays a crucial role in influencing cell behavior, indicating that the variation in size and spacing of synthetic guttae was detrimental to cell monolayer formation (19). Guttae was shown to trigger a stress response, cellular aging, epithelial-to-mesenchymal transition, and cellular apoptosis in a size-dependent manner. Kocaba et al. (19) observed that guttae with a mean diameter greater than 30 microns, significantly impeded endothelial monolayer formation, resulting in increased cell death and elevated expression of markers associated with endothelial to mesenchymal transition. In contrast, smaller guttae did not obstruct cell growth, allowing for better integration and function of transplanted CECs. This study highlighted the significant impact of guttae in endothelial degeneration and their potential to compromise otherwise healthy endothelial cells.

CECs situated in regions abundant in guttae exhibit increased rates of apoptosis, diminished mitochondrial mass, lower membrane potential, and elevated levels of intra-mitochondrial calcium (20). In response, CECs in areas with fewer guttae attempt to compensate by boosting their adenosine triphosphate (ATP) synthesis. However, this increase in ATP production subsequently leads to the generation of reactive oxygen species and results in oxidative stress (21). Multiple studies have demonstrated that guttae adversely impact adjacent CECs by affecting their mitochondrial function to the extent that the CECs undergo apoptosis. It remains uncertain whether guttae themselves are inherently toxic to CECs or if these changes stem from the compromised condition of CECs. Most likely, both mechanisms are at play: guttae may directly affect CECs, while the dysfunctional CECs secrete abnormal ECM proteins associated with guttae, altering their local microenvironment (20).


Commentary

Removing guttae from DM through surgical intervention before cell injection therapy may improve the likelihood of successful cultured CEC monolayer formation, thereby potentially enhancing treatment outcomes (18).

In their article in JAMA Ophthalmology, Tomioka et al. (22) have assessed the guttae behavior following cultured CEC transplant after removal of the degenerated CECs and the abnormal ECM. By removing the abnormal ECM components during surgery, the local microenvironment may be improved, facilitating better integration and function of transplanted cells.

The authors utilized a prospective observational design involving 15 eyes from patients with corneal endothelial failure due to FECD, monitoring changes in guttate morphology before and after surgery. The technique employed in this study involves scraping the abnormal ECM and degenerated CECs from the central 8 mm of the cornea, using a silicon cannula. The removal was confirmed by Vision Blue staining. A 300-µL suspension of cultured CECs was injected into the anterior chamber (11 received 1×106, 3 received 0.5×106 cells, and 1 received 0.2×106 cells), and the patients were positioned face down for 3 hours to facilitate cell adhesion.

The findings revealed that, post-surgery, there was a significant reduction in the number of guttae across different morphological classifications: typical, atypical, and absent guttae. Typical guttae were characterized by large guttae with no CECs above them. Atypical guttae had cells on their apical portion. No guttae were designated for eyes where the guttae themselves were very few.

The variability in the postoperative outcomes may correspond to multiple factors:

  • Different guttae dimensions (height, width, density) influence the migration, expansion, and monolayer formation of primary cells. Taller, wider, and high-density pillars have been found to be detrimental to cell monolayer formation (18).
  • Limitations of the imaging techniques utilized, in detecting the guttae and cells at various depths or heights.
  • Pathogenesis of FECD involves the formation of a posterior collagenous layer, which is composed of a posterior banded zone, and a posterior fibrillar zone (PFZ), in which the guttae can be buried (23,24). Hence, complete surgical removal of all the guttae may not be possible, as some may be buried in the PFZ, thus giving rise to variable surgical outcomes.

The authors mention that the guttae were removed by scraping with a silicone tip needle; however, in the specular microscopy images, it can be seen that almost 40% guttae recurred by 1-year postoperatively. This poses some interesting questions about this therapy in FECD.

The recurrence of guttae was comparatively less in the no guttae group, which showed a 16.2% recurrence in the early period with a slight increase to 18.8% in the late period. This is suggestive of the earlier clinical findings of injected CECs being able to form a monolayer on top of smaller guttae, such as those seen in earlier stages of FECD, as compared to larger guttae.

CEC injection (CECI) is likely to be more beneficial in the earlier stages of FECD, where guttae are smaller in size and density. Since guttae are predominantly found centrally, it may be better to limit the size of the scraped area. Although CECI is a promising solution, questions remain regarding its long-term efficacy and safety. Out of the 15 patients in this study, 11 received 1×106 cells. There are legitimate concerns about the theoretical risk of both inflammation associated with cellular aging, as well as the possibility of tumor formation by cells that do not adhere to the DM (25). Studies have successfully utilized less number of cells and a lower volume cell suspension (150–200 µL) (26,27). It is imperative that we deduce the optimum volume and number of cells to inject, that can be safely utilized and is cost-effective.

Post-injection anterior segment optical coherence tomography imaging of rabbit corneas has revealed that injected single cells form aggregated cellular clusters, which diminish over time (26). This suggests that multilayer CEC detached overtime and was cleared through the trabecular meshwork. Even though this could cause a raised intraocular pressure, this has not been found in both preclinical and clinical studies.

Most studies on outcomes of DM endothelial keratoplasty (DMEK) describe the results in the first 6–24 months postoperatively. In this study, early follow-up is defined as within 1 year. It is crucial to include the timeline from when the cellular monolayer aggregates become visible and monitor changes, including the period of guttae reappearance, as these factors are vital for assessing cellular functionality. In the no guttae group, we cannot definitively state that guttae disappeared. Guttae may initially not have been visible as they got blanketed in the injected CEC. While fewer guttae were observed in this group in the early postoperative period, there was a decline in the CEC density in the late postoperative period, likely due to the presence of guttae and its progressive toxic influence on even the healthy cultured CECs. Corneal clearing at later time points could also be due to host endothelial migration.

CEC density from an undetectable preoperative level had also increased in all three groups in the early postoperative period, with gradual decline over 3 years. The no guttae group exhibited the highest CEC density in both early and late phases, compared to the other two groups. The median percentage cell loss over 2 years from early to late postoperative period was 25%, 36%, and 20% for typical, atypical, and no guttae groups, respectively.

The results of CECI need to be at least comparable if not superior to DMEK. Studies by Birbal et al. (28) and Schlögl et al. (29), evaluating the long-term outcome of DMEK have reported a 5-year endothelial cell loss (ECL) of 51–59% and 44–49%, respectively after DMEK. The 10-year rates for these cohorts were 68–72%. Research has indicated that the most ECL takes place in the first 6 months following DMEK, with a continued linear decline in endothelial cell density (ECD) observed thereafter, typically ranging from 2.4% to 4.8% per year (28-30). Given the 3-year follow-up data of this study, the yearly ECL seems higher than what is seen after DMEK. The mean ECD is 3,369 and 2,468 cells/mm2 at year 1 and 3, respectively, which gives a yearly ECL of 8.9%. If we look at the three groups separately, the mean ECD at year 1 is 2,801/mm2, 3,265/mm2, and 4,558/mm2 and for year 3 is 1,933/mm2, 2,288/mm2, and 3,779/mm2 for typical, atypical, and no guttae groups, respectively. This gives a yearly ECL of 10.3% for the typical group, 9.98% for the atypical group, and 5.69% for the no guttae group.

The functionality of the CEC, in this study, was demonstrated by a reversal of corneal oedema and an improvement in best corrected visual acuity (BCVA). In the early postoperative period, 2-line improvement in BCVA was seen in 80% of eyes. In the other 20%, one patient developed posterior capsular opacification and the other had an anterior capsular contraction. Also, 80% had vision >20/40, 53.3% had >20/25 in the 1st postoperative year and by the 3rd postoperative year 60% had >20/25 vision and 40% had >20/20.

In comparison, DMEK delivers excellent and consistent visual acuity up to 2 years postoperatively with over 80% of eyes achieving a BCVA of ≥20/25 (≥0.8) and more than 50% reaching ≥20/20 (≥1.0) (31). It has also been shown that DMEK yields excellent visual-acuity outcomes [0.05 logarithm of the minimum angle of resolution (logMAR)] a few months after surgery that is sustained for up to 5 years after DMEK (32).

Weller et al. (33) highlighted that variations in guttae structure might correlate with visual acuity outcomes, suggesting that not all guttae are equivalent in their impact on corneal health. This underscores the importance of characterizing guttae morphology when assessing the treatment option and its outcome.


Strengths and limitations

The findings from Tomioka et al. (22) offer valuable insights into potential new strategies for treating FECD. By demonstrating that surgical techniques can effectively manage guttae while preserving critical structures within the cornea, this research encourages further advent of less invasive treatment options that could reduce patient dependence on donor tissues.

A larger study size would enhance the statistical power and generalizability of findings, making the results more conclusive.

Injection of mature-differentiated CECs into the anterior chamber was seen to be associated with improved BCVA and decrease in central corneal thickness, however longer-term outcomes remain uncertain.

The classification into typical and atypical guttae suggests variability that may influence treatment outcomes. Further research is needed to understand how different guttae characteristics respond to surgical intervention. While initial results are promising, there remains a risk that guttae recur over time due to underlying disease progression or incomplete removal during surgery.


Conclusions

This study represents a significant advancement in our understanding and management of FECD. However, further research is necessary to address the limitations identified in this study and explore outcomes comprehensively.

As mentioned earlier, Rizwan et al. (18) have shown that the height and density of guttae may affect the formation of a CEC monolayer and that large guttae can be toxic to injected endothelial cells (18,19). Thus, to ensure guttae removal, DM may need to be stripped in FECD with significant guttae and cell-injection therapy may not be appropriate in severe stages of FECD. We may be able to better evaluate the characteristics of these guttae using upcoming imaging techniques to predict the success of cell-injection therapies.

Cell therapy using propagated primary human CECs offers an alternative to corneal transplantations, and demonstrating the functionality of the CECs is crucial for its validation. If guttata cannot be completely removed, disease progression will continue, resulting in cellular apoptosis and continued depletion of endothelial cells.

As we continue to refine our approaches to treating FECD, integrating surgical innovations with advancements in cellular therapies and imaging techniques will be crucial in improving patient outcomes and quality of life. Future research should continue to explore the complex interactions between guttae morphology and endothelial cell behavior to optimize a more cost-effective, safe, and less invasive treatment strategies for FECD patients.


Acknowledgments

None.


Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Annals of Eye Science. The article has undergone external peer review.

Peer Review File: Available at https://aes.amegroups.com/article/view/10.21037/aes-24-41/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://aes.amegroups.com/article/view/10.21037/aes-24-41/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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doi: 10.21037/aes-24-41
Cite this article as: Malhotra D, Mehta JS. Cultured human corneal endothelial cell-based therapy for treatment of Fuchs endothelial corneal dystrophy. Ann Eye Sci 2025;10:11.

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