Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0314719 (dry eye)
2,625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Second leading cause of blindness worldwide, glaucoma is an optic neuropathy related mainly but not exclusively to an increase of intraocular pressure. Angle closure glaucoma is related to a blockade of aqueous humor to the trabecular meshwork, whereas open-angle glaucoma is a degeneration of the trabecular meshwork, the filter that allows aqueous outflow from the eye. Many improvements have been made in terms of diagnosis, follow-up and treatments, although the treatment of glaucoma is restricted to control intraocular pressure, in order to prevent optic nerve degeneration or to stop the progression of the disease toward blindness. The first line therapy is based on topical medications that are administered for the whole life span. Although globally efficient, these treatments, and most likely the preservative included in the excipient to prevent bottle contamination, induce side effects in the long-term that may impair the quality of life, patient compliance or directly induce ocular surface changes like inflammatory cytokine release, or tear film destruction, with further dry eye disease and chronic inflammation. A large body of evidence has been accumulated, showing that benzalkonium chloride, the preservative mainly used, is toxic over the long run and plays a role in such ocular surface impairment. Therefore efforts have been made in the last decade to eliminate or replace this compound, providing safer therapies to the patients. Furthermore, the identification of chemokines as playing a role in the trabecular degeneration has open new directions for treating glaucoma. The blockade of one receptor of CXCL12 has been experimentally shown not only to decrease intraocular pressure but also to prevent trabecular cell degeneration. This is an innovative concept that could allow development of new treatments, more specifically targeting the disease at its onset, rather than attempting to reduce its progression in its later stages.
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PMID:[Glaucoma today: detection and therapeutic progress]. 2410 39

Dry eye symptoms are among the leading complaints in ophthalmology. Dry eye disease (DED) is associated with significant pain affecting quality of life. Cellular and molecular mechanisms underlying ocular pain associated with DED are not fully understood. In this study, we investigated the ocular surface of patients with DED using in vivo confocal microscopy (IVCM) to quantify corneal nerve density and its relation with corneal inflammation. Gene expression of the proinflammatory markers HLA-DR, IL-6, CXCL12, and CCL2 and the receptors CXCR4 and CCR2, as well as PENK (enkephalin precursor), was therefore quantified in conjunctival impression cytology specimens. Thirty-two patients with DED and 15 age-matched controls were included. Subbasal nerve density was significantly lower in DED patients compared to controls. IVCM analysis revealed that DED patients had a significantly higher corneal dendritic cell density compared to controls. Conjunctival impression cytology analysis revealed that HLA-DR, IL-6, CXCR4, and CCL2/CCR2 mRNA levels were significantly increased in DED patients compared to controls, whereas PENK mRNA levels were significantly decreased. Similar results were obtained in vitro on immortalized human conjunctiva-derived epithelial cells challenged with osmotic stress that mimics the DED condition. These results demonstrate that proinflammatory molecules and endogenous enkephalin have opposite gene regulation during DED.
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PMID:Proinflammatory Markers, Chemokines, and Enkephalin in Patients Suffering from Dry Eye Disease. 2967 32