Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the stromal keratitis caused by herpes simplex virus (HSV), the formation of new vessels is the essential step for the pathogenesis of keratitis. Inhibition of angiogenesis diminishes the formation of corneal lesion induced by HSV. Procedures which suppress angiogenesis are proposed as a valuable therapeutic approach to control HSK. The mechanism by which HSV ocular infection results in corneal angiogenesis is not understood. Recent reports identified anti-vascular endothelial growth factor (VEGF) as a molecule that is highly expressed in the HSV infected eye and clearly involved in angiogenesis. The advent of VEGF treatments marks a major advancement in the treatment of angiogenic eye disease. Off-label use of bevacizumab (Avastin), a recombinant humanized monoclonal antibody directed against VEGF, in some neovascular disorders of the eye has been associated with promising short term results. Based on these evidences herein we hypothesize topical application of bevacizumab could inhibit corneal neovascularization and also scarring in HSK. We propose this drug as a novel adjunct to current anti-inflammatory strategies in HSK.
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PMID:Therapeutic potential of bevacizumab (Avastin) in herpetic stromal keratitis (HSK). 1736 59

Mitochondria play a role of energy production and produce intracellular reactive oxygen species (ROS), especially superoxide anion (O2(-)) as a byproduct of energy metabolism at the same time. O2(-) is converted from oxygen and is overproduced by excessive electron leakage from the mitochondrial respiratory chain. It is well known that mitochondrial complexes I and III in the electron transport system are the major endogenous ROS sources. We have previously demonstrated that mutations in complex II can result in excessive ROS (specifically in SDHC: G71E in Caenorhabditis elegans, I71E in Drosophila and V69E in mouse). Moreover, this results in premature death in C. elegans and Drosophila as well as tumorigenesis in mouse embryonic fibroblast cells. In humans, it has been reported that mutations in SDHB, SDHC or SDHD, which are the subunits of mitochondrial complex II, often result in inherited head and neck paragangliomas (PGLs). Recently, we established Tet-mev-1 conditional transgenic mice using our uniquely developed Tet-On/Off system, which can induce the mutated SDHC gene to be equally and competitively expressed compared to the endogenous wild-type SDHC gene. These mice experienced mitochondrial respiratory chain dysfunction that resulted in oxidative stress. The mitochondrial oxidative stress caused excessive apoptosis in several tissues leading to low-birth-weight infants and growth retardation during neonatal developmental phase in Tet-mev-1 mice. Tet-mev-1 mice also displayed precocious age-dependent corneal physiological changes, delayed corneal epithelialization, decreased corneal endothelial cells, thickened Descemet's membrane and thinning of parenchyma with corneal pathological dysfunctions such as keratitis, Fuchs' corneal dystrophy (FCD) and probably keratoconus after the normal development and growth phase. Here, we review the relationships between mitochondrial oxidative stress and phenomena in mev-1 animal models with mitochondrial complex II SDHC mutations. This article is part of a Special Issue entitled: Respiratory complex II: Role in cellular physiology and disease.
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PMID:Model animals for the study of oxidative stress from complex II. 2314 69