macular degeneration/protease

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Proteomics-based identification and validation of novel plasma biomarkers phospholipid transfer protein and mannan-binding lectin serine protease-1 in age-related macular degeneration.

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Age-related macular degeneration (AMD) is a major cause of severe, progressive visual loss among the elderly. There are currently no established serological markers for the diagnosis of AMD. In this study, we carried out a large-scale quantitative proteomics analysis to identify plasma proteins that

The role of proteases and inflammatory molecules in triggering neovascular age-related macular degeneration: basic science to clinical relevance.

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Age-related macular degeneration (AMD) causes severe vision impairment in aged individuals. The health impact and cost of the disease will dramatically increase over the years, with the increase in the aging population. Currently, antivascular endothelial growth factor agents are routinely used for

HTRA1, an age-related macular degeneration protease, processes extracellular matrix proteins EFEMP1 and TSP1.

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High-temperature requirement protein A1 (HTRA1) is a serine protease secreted by a number of tissues including retinal pigment epithelium (RPE). A promoter variant of the gene encoding HTRA1 is part of a mutant allele that causes increased HTRA1 expression and contributed to age-related macular

HTRA1 Overexpression Induces the Exudative Form of Age-related Macular Degeneration.

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Age-related macular degeneration (AMD) is a leading cause of vision loss and blindness in the elderly. The dry form is more common and accounts for about 85-90% of AMD patients in US, while Japanese AMD patients predominantly progress to wet-form or polypoidal choroidal vasculopathy (PCV). Recent

Subretinal new vessel recurrence in age-related macular degeneration.

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Laser photocoagulation with argon or krypton is currently used to treat selected patients with age-related macular degeneration and sudden visual loss from subretinal new vessel formation. In 102 consecutive cases, treated over two years, closure of the vessels was achieved without additional major

Met72Thr polymorphism of pigment epithelium-derived factor gene and susceptibility to age-related macular degeneration.

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Age-related macular degeneration (ARMD) is the most common cause of acquired blindness among the people of occupational age. Although the pathogenesis of ARMD is not fully understood, several studies suggest a possible contribution of a genetic factor in the development and progression of ARMD.

VEGF rescues cigarette smoking-induced human RPE cell death by increasing autophagic flux: implications of the role of autophagy in advanced age-related macular degeneration.

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OBJECTIVE Cigarette smoking (CS) is the most consistent risk factor for advanced age-related macular degeneration (AMD). To verify the molecular basis for CS-induced RPE alterations, RPE cell survival levels after being exposed to CS in relation with VEGF expression and autophagic flux were

Progress in defining the molecular biology of age related macular degeneration.

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Age related macular degeneration (AMD) is an extremely prevalent complex genetic disorder. Its incidence rises exponentially in the elderly to a frequency of 1 in 2 in the general population by age 85. It affects approximately 25 million people and is the commonest cause of irreversible visual loss

Modulation of the proteolytic activity of the complement protease C1s by polyanions: implications for polyanion-mediated acceleration of interaction between C1s and SERPING1.

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The complement system plays crucial roles in the immune system, but incorrect regulation causes inflammation and targeting of self-tissue, leading to diseases such as systemic lupus erythematosus, rheumatoid arthritis and age-related macular degeneration. In vivo, the initiating complexes of the

Secreted leukocyte protease inhibitor is present in aqueous humours from cataracts and other eye pathologies.

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Previous studies identified serine, cysteine and metalloproteases in normal aqueous humours (AH) and suggested that a balance between proteases and their inhibitors may play a role in the modulation of the AH outflow. We aimed to determine whether secretory leukocyte protease inhibitor (SLPI), a

Structure-Based Library Design and Fragment Screening for the Identification of Reversible Complement Factor D Protease Inhibitors.

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Chronic dysregulation of alternative complement pathway activation has been associated with diverse clinical disorders including age-related macular degeneration and paroxysmal nocturnal hemoglobinurea. Factor D is a trypsin-like serine protease with a narrow specificity for arginine in the P1

Light induces programmed cell death by activating multiple independent proteases in a cone photoreceptor cell line.

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OBJECTIVE Although the apoptotic death of photoreceptor cells in retinal degenerative disorders is well documented, the molecular mechanism is not understood. The objective of this study was to determine the molecular events leading to the death of photoreceptor cells. METHODS An assay was developed

Role of Protease-Inhibitors in Ocular Diseases.

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It has been demonstrated that the balance between proteases and protease-inhibitors system plays a key role in maintaining cellular and tissue homeostasis. Indeed, its alteration has been involved in many ocular and systemic diseases. In particular, research has focused on keratoconus, corneal

Protoporphyrins enhance oligomerization and enzymatic activity of HtrA1 serine protease.

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High temperature requirement protein A1 (HtrA1), a secreted serine protease of the HtrA family, is associated with a multitude of human diseases. However, the exact functions of HtrA1 in these diseases remain poorly understood. We seek to unravel the mechanisms of HtrA1 by elucidating its

Two genetic pathways for age-related macular degeneration.

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The discovery of strong associations of the His402 variant of complement factor H (CFH) and the change in the promoter region of HtrA serine peptidase 1 (HTRA1) with age-related macular degeneration (AMD) have altered our conception of the pathophysiology of this disease. The complement system has

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