Surgical strategies to improve visual outcomes in corneal transplantation

The recent years have brought about a sea change in the field of corneal transplantation with penetrating keratoplasty being phased to newer lamellar keratoplasty techniques for a variety of corneal pathology. Improved and innovative surgical techniques have allowed selective replacement of diseased host corneal layers with pre-prepared healthy donor corneal lamellae for anterior corneal disorders such as keratoconus and posterior corneal disorders such as Fuch''s corneal endothelial dystrophy. The results of lamellar techniques are encouraging, with rapid visual rehabilitation and vastly reduced risk of immune-mediated transplant rejection. The techniques of deep anterior lamellar keratoplasty and Descemet''s stripping endothelial keratoplasty (DSAEK) continue to evolve with advent of femtosecond lasers and newer concepts such as pre-conditioned donor corneas for Microthin DSAEK and Descemet''s membrane keratoplasty. This review describes the current developments in lamellar keratoplasty, including the futuristic approach using cell therapy to restore vision in corneal blindness.     

Four in one: Four recepients with a single donor tissue - A novel concept for eye transplantation surgery post-COVID-19

A donor corneo-scleral button was dissected into four parts using a simple manual technique. The anterior corneal lamellae was stripped from the Descemet''s Membrane (DM) and Deep Anterior Lamellar Keratoplasty (DALK) was performed in a patient with advanced keratoconus after removing the recipient''s stroma using the big bubble technique. Descemet''s Membrane Endothelial Keratoplasty (DMEK) was done with the stripped donor DM in a patient with Fuch''s endothelial dystroph (FECD). The cadaveric limbal stem cells from the tissue were used for simple limbal epithelial transplantation (SLET) in a Steven- Johnson Syndrome (SJS) with localized limbal stem deficiency and symblepharon. The sclera was used to revise a leaking hypotonus bleb in an advanced single-eyed glaucoma patient. No intraoperative or postoperative complications were observed. At 1 year, all the 4 cases retained healthy transplanted tissues with good visual outcomes. Shortage of donor eyes is a global problem and with the present COVID-19 scenario the situation is bound to worsen. The advent of customized component corneal transplantation using simple cost-effective techniques will be the future trend in the years to come.     

Rho-associated kinase inhibitors: A novel glaucoma therapy

The rho-associated kinase (ROCK) signaling pathway is activated via secreted bioactive molecules or via integrin activation after extracellular matrix binding. These lead to polymerization of actin stress fibers and formation of focal adhesions. Accumulating evidence suggests that actin cytoskeleton-modulating signals are involved in aqueous outflow regulation. Aqueous humor contains various biologically active factors, some of which are elevated in glaucomatous eyes. These factors affect aqueous outflow, in part, through ROCK signaling modulation.Various drugs acting on the cytoskeleton have also been shown to increase aqueous outflow by acting directly on outflow tissue. In vivo animal studies have shown that the trabecular meshwork (TM) actin cytoskeleton in glaucomatous eyes is more disorganized and more randomly oriented than in non-glaucomatous control eyes. In a previous study, we introduced ROCK inhibitors as a potential glaucoma therapy by showing that a selective ROCK inhibitor significantly lowered rabbit IOP. Rho-associated kinase inhibitors directly affect the TM and Schlemm's canal (SC), differing from the target sight of other glaucoma drugs. The TM is affected earlier and more strongly than ciliary muscle cells by ROCK inhibitors, largely because of pharmacological affinity differences stemming from regulatory mechanisms. Additionally, ROCK inhibitors disrupt tight junctions, result in F-actin depolymerization, and modulate intracellular calcium level, effectively increasing SC-cell monolayer permeability.Perfusion of an enucleated eye with a ROCK inhibitor resulted in wider empty spaces in the juxtacanalicular (JCT) area and more giant vacuoles in the endothelial cells of SC, while the endothelial lining of SC was intact. Interestingly, ROCK inhibitors also increase retinal blood flow by relaxing vascular smooth muscle cells, directly protecting neurons against various stresses, while promoting wound healing. These additional effects may help slow progressing visual field loss in glaucoma patients, making ROCK inhibitors an even more desirable anti-glaucoma agent. All evidence indicates that aqueous humor outflow is affected by cytoskeleton physiology and this information may provide valuable insight into understanding glaucoma pathology and treatment.     

DIFFERENTIATION AND ASSESSMENT OF CORNEAL ENDOTHELIAL CHANGES ASSOCIATED WITH DISEASES OF THE ANTERIOR SEGMENT OF THE EYE

Recent work has shown changes in the corneal endothelium accompanying corneal epithelial disease and anterior uveitis. It is important to differentiate these acute changes from other changes such as guttatae or corneal pigment deposition and to assess the magnitude of their effect upon the corneal endothelium. We have used specular microscopy to study changes in the corneal endothelium and Descemet's membrane and to study deposits on the back of the corneal endothelium and correlate them with changes in the endothelium by the use of conventional specular microscopy and by relief images which give a three dimensional view of the area concerned. This has particularly been applied to the conditions of superficial punctate keratopathy, keratoconjunctivitis sicca, corneal abrasions and exposure keratopathy, iritis and cyclitis, pseudoexfoliation of the lens capsule, anterior sement pigment dispersal syndrome, bullous keratopathy as well as corneal guttatae and pigment granuis on the posterior cornea. freendothelial lesions have been distinguished from endothelial and retrocorneal lesions by this technique aiding elucidation of the state of the endothelium. The changes which we noted occurred either at the level of Descemet's membrane (including formation of small rounded dark blebs less than one cell in diameter, larger blebs one to three cells in diameter, and guttatae, usually larger than the foregoing and sometimes very numerous), or at the level of the posterior endothelial surface (including small shiny nodular deposits, often numerous. due to pigment granules, and keratitic precipitates and inflammatory debris, the former usually large and the latter smaller, more irregular and somethimes very numeroug The differentiation and assessment of these various changes are discussed.     

Intracorneal blood removal six weeks after canaloplasty

In a 71-year-old patient with bilateral open-angle glaucoma, intracorneal blood was found after a canaloplasty procedure in the right eye. Six weeks after surgery on ultrasound biomicroscopy examination, liquified blood and blood clots could be observed nasally in the deep corneal stroma close to the Descemet''s membrane. The intracorneal blood was washed out with balanced saline solution following deep corneal incision and lamellar dissection. Descemet''s membrane was reattached with air injection into the anterior chamber. Two months later, visual acuity improved to 20/50, intraocular pressure was 16 mm Hg without medication and confocal microscopy showed deep stromal folds and limited endothelial cell loss. Viscoelastic entering the cornea at Schwalbe''s line and reflux of blood from the collector channels to Schlemm''s canal can account for corneal hematoma. Even six weeks after canaloplasty, successful blood removal could be fulfilled without rupturing the Descemet''s membrane.     

Evaluation of the effects of circular Descemet's membrane incision on the biomechanical, topographic and optical properties of rabbit corneas

Background: Prospective interventional animal case series to investigate quantitatively changes in corneal light‐scattering, corneal hysteresis, keratometry and pachymetry induced by circular Descemet's membrane incision. Methods: Thirty mature New Zealand White rabbits were divided into three study groups: (i) surgical intervention with circular Descemet's incision; (ii) surgical control; and (iii) medical control. Group 1 eyes had two paracenteses placed 120 degrees apart and an 8.5‐mm‐diameter Descemetorhexis was created with a reverse Sinskey hook. Group 2 eyes had two paracenteses placed 120 degrees apart. The main outcome measures were scatterometry, corneal hysteresis, pachymetry and keratometry measurements, which were performed prior to and 2 weeks following the interventions. Histology and transmission electron microscopy were performed post‐mortem in representative eyes. Results: Eyes that had undergone circular Descemet's incision had significantly decreased mean keratometry (43.9 ± 0.7 dioptres [mean ± standard deviation] preoperatively vs. 43.5 ± 0.9 dioptres postoperatively, P = 0.007). Circular Descemet's membrane incision did not significantly change corneal hysteresis (4.4 ± 1.1 mmHg preoperatively vs. 4.6 ± 0.9 mmHg postoperatively, P = 0.664). Corneal light scattering decreased after Descemet's scoring (0.00254 ± 0.00059 preoperatively vs. 0.00206 ± 0.00031 postoperatively, P = 0.0025). Pachymetry measurements remained relatively stable (341.3 ± 18.6 µm preoperatively vs. 330.6 ± 20.0 µm postoperatively) without postoperative oedema. Conclusions: Circular Descemet's scoring flattened the corneal curvature by a mean of 0.4 dioptres without affecting corneal hysteresis in rabbit corneas. These findings may have important implications for ongoing developments in endothelial keratoplasty.     

微环境对角膜内皮作用机制的研究进展

角膜内皮作为角膜中代谢最为活跃的一层,在维持角膜透明性中发挥重要作用.角膜内皮微环境则是揭示角膜内皮疾病机制和体外培养角膜内皮进而解决角膜内皮移植供体匮乏的关键,其包括了普遍存在的,对细胞有直接作用的生长因子、营养因子、炎性因子及干性因子等各种细胞因子.同时因角膜内皮位置特异性所形成的高氧化环境、眼压等物理应力及相邻组织,如晶状体、角膜后弹力层、房水等与角膜内皮的相互作用也是微环境中的重要因素     

Development of new therapeutic modalities for corneal endothelial disease focused on the proliferation of corneal endothelial cells using animal models

This review describes our recent attempts to develop new therapeutic modalities for corneal endothelial disease using animal models including non-human primate model in which the proliferative ability of corneal endothelial cells is severely limited, as is the case in humans. First, we describe our attempt to develop new surgical treatments using cultivated corneal endothelial cells for advanced corneal endothelial dysfunction. It includes two different approaches; a "corneal endothelial cell sheet transplantation" with cells grown on a type-I collagen carrier, and a "cell-injection therapy" combined with the application of Rho-kinase (ROCK) inhibitor. Recently, it was reported that the selective ROCK inhibitor, Y-27632, promotes cell adhesion and proliferation and inhibits the apoptosis of primate corneal endothelial cells in culture. When cultivated corneal endothelial cells were injected into the anterior chamber of animal eyes in the presence of ROCK inhibitor, endothelial cell adhesion was promoted and the cells achieved a high cell density and a morphology similar to corneal endothelial cells in?vivo. We are also trying to develop a novel medical treatment for the early phase of corneal endothelial disease by the use of ROCK inhibitor eye drops. In rabbit and monkey experiments using partial endothelial dysfunction models, corneal endothelial wound healing was accelerated by the topical application of ROCK inhibitor to the ocular surface, and resulted in the regeneration of a corneal endothelial monolayer with a high endothelial cell density. We are now trying to advance the clinical application of these new therapies for patients with corneal endothelial dysfunction.     

Impact of the clinical use of ROCK inhibitor on the pathogenesis and treatment of glaucoma

Rho-associated protein kinase (ROCK), a ubiquitously expressed signaling messenger and downstream effector of Rho, is activated by several bioactive factors in the aqueous humor (AH). Rho-ROCK signaling regulates a wide spectrum of fundamental cellular events, including cell adhesion, motility, proliferation, differentiation, and apoptosis. Previous studies, including our own, found that ROCK inhibitor lowers intraocular pressure (IOP) via a direct effect on the conventional AH outflow pathway, by regulation of contractile properties, fibrotic activity, and permeability of the trabecular meshwork (TM) and Schlemm’s canal (SC) tissues, influencing extracellular matrix (ECM) production. Recently, a novel ROCK inhibitor, ripasudil, has been introduced in Japan. Other ROCK inhibitors are now in clinical trials as new IOP-lowering drugs for glaucoma patients. To date, ripasudil, administered together with other glaucoma medications, has proved safe and efficient in lowering IOP as well as additional effects such as prostaglandin analogs, beta-blockers, and carbonic anhydrase inhibitors, all of which help lower IOP by different mechanisms. In addition, we found that long-term treatment with ripasudil exerted an additional IOP-lowering effect, especially in eyes with high IOP, suggesting that late-onset remodeling of the ECM in glaucomatous eyes may elicit mild and delayed changes in IOP levels. ROCK inhibitors have also shown several additional effects, including increased retinal blood flow, direct protection of neurons against various types of stress, and regulation of wound healing; these benefits may potentially be useful in glaucoma treatment.     

New understanding and development of medical treatments for ocular diseases based upon molecular mechanisms

A number of genes associated with life phenomena have been identified by the achievement of genome projects. As both comprehensive analysis and methods for investigation of specific genes have been developed, we can understand the pathogenesis of ocular diseases and develop novel medical treatments based upon detailed information on molecular mechanisms. In our review article, we focused on three vision-threatening ocular diseases; glaucoma, age-related macular degeneration (AMD) and proliferative vitreoretinopathy (PVR), and discussed the potential and problems related to retinal regenerative therapy. Regarding glaucoma, we investigated the relationships between aqueous humor and cell components in the aqueous outflow route. We have revealed that the Rho-Rho-associated coiled-coil-forming protein kinase (ROCK) signal transduction pathway participates in regulation of the aqueous outflow route, and that ROCK inhibitors and several protein kinase inhibitors exert intraocular pressure-lowering effects. Also, we conducted a series of investigations on familial amyloidotic polyneuropathy (FAP), as a representative secondary glaucoma caused by genetic mutations in a single gene. We reviewed the clinical features of ocular complications derived from FAP, their molecular mechanisms and possibilities for the development of novel medical treatments. In addition, we discussed a novel therapeutic concept, "neuroprotection", and showed the potential of some drugs as candidates for the neuroprotective treatment of glaucoma. Against AMD, we have performed a series of experiments from the viewpoint of similarity with atherosclerotic lesions. We have shown the molecular mechanisms of AMD associated with up-regulated expression of scavenger receptors and the interaction between leukocytes and vascular endothelial cells. Furthermore, in the pathogenesis of PVR, we described the role of epithelial-mesenchymal transition in retinal pigment epithelial cells and demonstrated the usefulness of enzymatic vitrectomy. Although retinal regenerative therapy has attracted much attention from global investigators, we pointed out its limitation for clinical application, and developed researches on efficient culture method using physiologically active factors for proliferating retinal stem cells with multi-potentiality, differentiation of the transplanted progenitor cells, and axon guidance of neurons by extracellular matrices.     

A Case of Bilateral Descemet's Membrane and Subepithelial Opacity: In vivo Laser Confocal Microscopic Study

Purpose

To report the in vivo laser confocal microscopy findings from a patient with Descemet''s membrane and subepithelial opacity OU.

Case Report

A healthy 41-year-old male with Descemet''s membrane and subepithelial opacity OU was studied. Routine ophthalmic examination, standard slit-lamp biomicroscopy, and in vivo laser confocal microscopic analysis of the entire corneal layer were performed. Slit-lamp biomicroscopy revealed subepithelial opacity in the mid-peripheral to peripheral cornea and numerous opacities located at the level of Descemet''s membrane. It was difficult to distinguish the precise histological location of the opacity. In vivo laser confocal microscopy showed numerous hyperreflective particles in the subepithelium to superficial stroma and hyperreflectivity of Descemet''s membrane. No abnormalities could be detected in the epithelial cell layer, midstromal layer, deep stromal layer, or endothelial cell layer.

Conclusion

Although the origin of the corneal opacities was unclear, in vivo laser confocal microscopy was useful for observing microstructural abnormalities in a case of Descemet''s membrane and subepithelial opacity.Key words: Descemet''s membrane opacity, Subepithelial opacity, Confocal microscopy     

High Glucose Aggravates Retinal Endothelial Cell Dysfunction by Activating the RhoA/ROCK1/pMLC/Connexin43 Signaling Pathway

PurposeThis research aims to explore the mechanism underlying the relationship between RhoA/ROCK signaling and Connexin43 (Cx43) in retinal endothelial cell dysfunction and to evaluate the protective effect of ROCK inhibitors against retinal endothelial cell dysfunction in diabetic retinopathy (DR) models.MethodsTUNEL staining, hematoxylin and eosin staining, a retinal digestion assay, and Evans blue assay were conducted to explore the effect of fasudil in alleviating retinal dysfunction induced by DR. ELISA, the CCK-8 assay, and flow cytometry were conducted to study inflammation, viability, and apoptosis of mouse retinal microvascular endothelial cells treated with high glucose and ROCK inhibitors. The qRT–PCR and Western blotting were used to evaluate the expression of RhoA, ROCK1, ROCK2, MLC, pMLC, and Cx43. Co-immunoprecipitation was used to verify the interaction between pMLC and Cx43. Immunofluorescence and scrape-loading and dye transfer were used to evaluate the expression and function of Cx43.ResultsMarked endothelial cell dysfunction resulting from the activation of RhoA/ROCK1 signaling was found in in vivo and in vitro models of DR. Via interaction with pMLC, which is downstream of RhoA/ROCK1, a significant downregulation of Cx43 was observed in retinal endothelial cells. Treatment with ROCK inhibitors ameliorated retinal endothelial dysfunction in vitro. The ROCK inhibitor, fasudil, significantly alleviated retinal dysfunction as shown by a decrease of retinal acellular capillaries, an improvement of vascular permeability, and a reduction of cell apoptosis in vivo.ConclusionsOur study highlights a novel mechanism that high glucose could activate RhoA/ROCK1/pMLC signaling, which targets the expression and localization of Cx43 and is responsible for cell viability, apoptosis, and inflammation, resulting in retinal endothelial cell injury. ROCK inhibitors markedly ameliorate endothelial cell dysfunction, suggesting their therapeutic potential for diabetic retinopathy.     

Interference of Descemet's Membrane with Aqueous Humor Drainage via an ExPRESS Mini Shunt

Purpose

To describe a case in which Descemet''s membrane interfered with aqueous humor drainage through an ExPRESS mini shunt. This problem was successfully solved by Nd:YAG laser membranotomy.

Case Report

A 70-year-old male, diagnosed with corticosteroid-induced glaucoma in his right eye, presented to our hospital. Topical betamethasone treatment was discontinued, and the patient was treated with intravenous D-mannitol and acetazolamide, followed by oral acetazolamide, oral potassium L-aspartate, topical dorzolamide hydrochloride, topical carteolol hydrochloride, and topical latanoprost. However, his right intraocular pressure (IOP) remained elevated. We performed ExPRESS shunt surgery in the patient''s right eye. His postoperative IOP was initially within the normal range, but it reincreased 1 month after surgery. We found that the Descemet''s membrane was interfering with both the primary (axial) and reserve orifices at the tip of the ExPRESS mini shunt. Nd:YAG laser membranotomy was performed and the patient''s IOP again improved without any other medical treatment.

Conclusion

Descemet''s membrane interfered with aqueous humor drainage via ExPRESS mini shunt, causing an increased IOP, which was resolved by Nd:YAG laser membranotomy.Key words: Corticosteroid-induced glaucoma, Descemet''s membrane, ExPRESS mini shunt     

Non-ulcerative infiltrative keratitis in RGP daily wear – a case report

A 61 -year-old female patient wearing rigid gas permeable (RGP) lenses on a daily basis presented with considerable pain and hyperaemia in the right eye. Biomicroscopic examination revealed marked stromal and endothelial oedema with folds in Descemet's membrane, and a focal infiltrate near the inferior limbus. The infiltrate was diagnosed as sterile on the basis of an intact overlying epithelium, lack of discharge and anterior chamber reaction, and the peripheral location. Considering the size and superficial nature of the infiltrate, the pain and corneal oedema were disproportionately severe. Differential diagnosis and management of sterile infiltrative keratitis are discussed using this case as an example.     

Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis

Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto(mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.     

Corneal Opacity: Cell Biological Determinants of the Transition From Transparency to Transient Haze to Scarring Fibrosis,and Resolution,After Injury

PurposeTo highlight the cellular, matrix, and hydration changes associated with opacity that occurs in the corneal stroma after injury.MethodsReview of the literature.ResultsThe regulated transition of keratocytes to corneal fibroblasts and myofibroblasts, and of bone marrow-derived fibrocytes to myofibroblasts, is in large part modulated by transforming growth factor beta (TGFβ) entry into the stroma after injury to the epithelial basement membrane (EBM) and/or Descemet''s membrane. The composition, stoichiometry, and organization of the stromal extracellular matrix components and water is altered by corneal fibroblast and myofibroblast production of large amounts of collagen type I and other extracellular matrix components—resulting in varying levels of stromal opacity, depending on the intensity of the healing response. Regeneration of EBM and/or Descemet''s membrane, and stromal cell production of non-EBM collagen type IV, reestablishes control of TGFβ entry and activity, and triggers TGFβ-dependent myofibroblast apoptosis. Eventually, corneal fibroblasts also disappear, and repopulating keratocytes reorganize the disordered extracellular matrix to reestablish transparency.ConclusionsInjuries to the cornea produce varying amounts of corneal opacity depending on the magnitude of cellular and molecular responses to injury. The EBM and Descemet''s membrane are key regulators of stromal cellularity through their modulation of TGFβ. After injury to the cornea, depending on the severity of the insult, and possibly genetic factors, trace opacity to severe scarring fibrosis develops. Stromal cellularity, and the functions of different cell types, are the major determinants of the level of the stromal opacity.     

Glaucoma-associated corneal endothelial cell damage: A review

The corneal endothelium is critical in maintaining a healthy and clear cornea. Corneal endothelial cells have a significant reserve function, but preservation of these cells is paramount as they have limited regenerative capacity. Glaucoma is a prevalent disease, and damage to the corneal endothelium may be caused by the disease process itself as well as by its treatment. The mechanisms involved in glaucoma-associated damage to the corneal endothelium need further investigation. Understanding how glaucoma and glaucoma surgery impact the endothelium is important for protecting corneal clarity and visual acuity in all glaucoma patients, including those undergoing corneal transplant. We will discuss a range of identified factors that may impact corneal endothelial cell health in glaucoma, including intraocular pressure, glaucoma medications, surgical glaucoma management, mechanical forces, and alterations in the aqueous environment.     

白内障术后角膜后弹力层脱离的临床观察

目的：探讨白内障超声乳化联合人工晶状体植入术及白内障囊外摘除联合人工晶状体植入术所致角膜后弹力层脱离的原因及有效诊疗方法。

方法：回顾性分析2015-01/2017-12在我院行白内障超声乳化联合人工晶状体植入术或白内障囊外摘除联合人工晶状体植入术的2 006例2 069眼,对术中或者术后发生角膜后弹力层脱离的26例26眼患者的诊疗及预后进行临床观察。

结果：发生不同程度角膜后弹力层脱离的26例26眼患者经相应治疗,未发生角膜内皮失代偿。角膜水肿消退,恢复透明,视力不同程度地提升。UBM检查证实后弹力层复位。

结论：白内障术中术后及时发现,根据不同情况选择合适的治疗方法,是治疗白内障术后角膜后弹力层脱离,恢复患者视力的关键。     

The new therapeutic concept of using a rho kinase inhibitor for the treatment of corneal endothelial dysfunction

Corneal endothelial cells (CECs) show poor regenerative ability in humans, and noncompensatory damage of CECs causes irreversible corneal haziness in cases of bullous keratopathy. Although corneal transplantations provide considerable clinical benefits, allograft rejection, primary graft failure, and the shortage of donor corneas are problems that still need to be overcome. The establishment of new treatment therapies is the key to solving these problems, and we have attempted to establish a new clinical intervention for corneal endothelial dysfunction. We previously demonstrated that the inhibition of Rho/Rho kinase (ROCK) signaling by Y-27632, a specific ROCK inhibitor, promoted cell adhesion, inhibited apoptosis, and enhanced cell proliferation in cultured primate CECs. These results raise the possibility that the ROCK inhibitor might serve as a new tool for establishing an effective culture method for newly emerging cultivated CEC transplantation therapies. Moreover, because Y-27632 enhances cell proliferation in vitro, we hypothesized that the use of a ROCK inhibitor could be a new pharmacological intervention for the treatment of corneal endothelial dysfunction. We demonstrated that the topical instillation of a ROCK inhibitor promotes corneal endothelium wound healing in an animal model. This indicates that use of a ROCK inhibitor is a less invasive and novel therapy that should prove promising for the treatment of corneal endothelial dysfunction.     

虹膜角膜内皮综合征的治疗新进展

虹膜角膜内皮综合征（ iridocorneal endothelial syndrome, ICES）是临床上比较少见的眼部疾病之一,其发病机制尚不明确,症状复杂,有很高的致盲率。患者常因青光眼、视力减退、眼痛和虹膜异常来就诊。 ICES至今尚无理想的治疗方法,临床上只能针对其并发症采取相应的药物、手术治疗。本文将对近期有关ICES治疗进展的文献进行综述,同时对极易出现误诊的疾病进行鉴别,以期对ICES的治疗提供帮助。