Effects of Synthetic Inhibitor of Metalloproteinase and Cyclosporin A on Corneal Haze after Excimer Laser Photorefractive Keratectomy in Rabbits

Chang, Jin Ho; Kook, Myeong Cherl; Lee, Jin Hak; Chung, Hum; Wee, Won Ryang

doi:10.1006/exer.1997.0415

Cited by 18 publications

(10 citation statements)

References 27 publications

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“…have shown some benefit in animal studies. However, their high toxicity combined with other deleterious side effects limit their use in humans [98–100]. Nerve growth factor and amniotic membrane have also been reported to control corneal scar and corneal ulcer formation.…”

Section: Current and Future Treatments Targeting Tgfβmentioning

confidence: 99%

Role of Transforming Growth Factor Beta in Corneal Function, Biology and Pathology

Tandon¹,

Tovey²,

Sharma³

et al. 2010

CMM

155

157

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Transforming growth factor-beta (TGFβ) is a pleiotropic multifunctional cytokine that regulates several essential cellular processes in many parts of the body including the cornea. Three isoforms of TGFβ are known in mammals and the human cornea expresses all of them. TGFβ1 has been shown to play a central role in scar formation in adult corneas whereas TGFβ2 and TGFβ3 have been implicated to play a critical role in corneal development and scarless wound healing during embryogenesis. The biological effects of TGFβ in the cornea have been shown to follow SMAD dependent as well as SMAD-independent signaling pathways depending upon cellular responses and microenvironment. Corneal TGFβ expression is necessary for maintaining corneal integrity and corneal wound healing. On the other hand, TGFβ is perhaps the most important cytokine in the pathogenesis of fibrotic disease in the cornea. Although the transformation of keratocytes to myofibroblasts induced by TGFβ is largely believed to cause corneal fibrosis or scarring, the precise molecular mechanism(s) involved in this process is still unknown. Currently no drugs are available to treat corneal scarring effectively without causing significant side effects. Many approaches to treat TGFβ-mediated corneal scarring are under investigation. These include blocking of TGFβ, TGFβ receptor, TGFβ function and/or TGFβ maturation. Other strategies such as modulating keratocyte proliferation, apoptosis, transcription and DNA condensation are also being investigated. The potential of gene therapy to neutralize the pathologic effects of TGFβ has also been demonstrated recently.

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Section: Current and Future Treatments Targeting Tgfβmentioning

confidence: 99%

Role of Transforming Growth Factor Beta in Corneal Function, Biology and Pathology

Tandon¹,

Tovey²,

Sharma³

et al. 2010

CMM

155

157

View full text Add to dashboard Cite

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“…The over expression of metalloproteinase-3 (MMP-3) (stromelysin-1) and MMP-13 (collagenase-3) is associated with non-healing wounds, whereas active MMPs-1, -2, -9, and -14 are required for normal wound healing to occur [64,95,96]. The synthetic metalloproteinase inhibitor, HSCH2CH[CH2CH(CH3)2] CO-Phe-Ala-NH2 (SIMP) is effective in neutralizing the metalloprotease MMP-3 and MMP-13, but not MMPs-1, -2, -9 and -14 [97]. Therefore, SIMP can be used to eliminate MMP-3 and -13, while allowing normal wound healing to take place [97].…”

Section: Metalloproteinase Inhibitors: Synthesis and Suppression Of Imentioning

confidence: 99%

“…The synthetic metalloproteinase inhibitor, HSCH2CH[CH2CH(CH3)2] CO-Phe-Ala-NH2 (SIMP) is effective in neutralizing the metalloprotease MMP-3 and MMP-13, but not MMPs-1, -2, -9 and -14 [97]. Therefore, SIMP can be used to eliminate MMP-3 and -13, while allowing normal wound healing to take place [97].…”

Section: Metalloproteinase Inhibitors: Synthesis and Suppression Of Imentioning

confidence: 99%

Techniques for Wound Healing with a Focus on Pressure Ulcers Elimination

Kuffler¹

2012

TOCVJ

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Pressure ulcers, also called decubitus ulcers, are a common challenge of humanity. They are wounds initiated by pressure on the skin that blocks circulation causing the skin and underlying tissues to die. Without care, pressure ulcers continue to grow in diameter and depth and are exceptionally difficult to heal. They have probably always existed, and are present on Egyptian mummies. Pressure ulcers are a serious health issue, very painful, a significant physiological challenge, can shorten the life of a patient, are an emotional and financial burden to the patient, those who deal with them, and in the United States alone annually costs in excess over $10 billion dollars for care and prolonged hospitalization. Pressure ulcers can develop with as little as two hours of pressure, and because even a brief lapse in avoidance of pressure leads to ulcers, they are frequently impossible to prevent, even for the most conscientious patient with an extensive support group and unlimited financial resources. Therefore, enormous effort is required to find effective and reliable techniques for preventing the initiation of ulcers and eliminating them once they develop. This review looks at the various approaches presently used and in development for the treatment of pressure ulcers, evaluates which may be best in eliminating ulcers, and discusses combinations of techniques that may be most effective in eliminating pressure ulcers.

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“…30 The use of topical collagenase inhibitors or synthetic inhibitor of metalloproteinase were also proposed, but their clinical use is still doubtful because of their side effects or little effectiveness. [31][32] Mitomycin-C (MMC), a highly cornea. Three to 4 layers of epithelial cells were observed and keratocytes were shown to be distributed regularly in all stromal layers.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, the mechanism of corneal haze and prophylactic therapies have been investigated, and new therapeutic agents have been proposed and tested. [26][27][28][29][30][31][32][33][34][35][36] Previous histologic studies indicated that corneal haze was restricted to the area directly beneath the ablated area and contained some atypical extracellular matrix components including type III, IV, and VII collagens, fibronectin, laminin, and tenascin, along with proteoglycans and proliferating keratocytes. 37-39 A variety of growth factors and cytokines including epidermal growth factor, keratinocyte growth factor, fibroblast growth factor, and vascular endothelial growth factor as well as TGFb are known to regulate this corneal stromal woundhealing process after PRK.…”

Section: Discussionmentioning

confidence: 99%