A
António F. Ambrósio
Researcher at University of Coimbra
Publications - 190
Citations - 6155
António F. Ambrósio is an academic researcher from University of Coimbra. The author has contributed to research in topics: Retina & Retinal. The author has an hindex of 42, co-authored 164 publications receiving 4886 citations. Previous affiliations of António F. Ambrósio include Vision-Sciences, Inc..
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TNF-α Signals Through PKCζ/NF-κB to Alter the Tight Junction Complex and Increase Retinal Endothelial Cell Permeability
TL;DR: In this article, the effects of IL-1β and TNF-α on retinal endothelial cell permeability were compared and the molecular mechanisms by which TNFα increases cell leakage were elucidated, which suggests that PKCζ may provide a specific therapeutic target for the prevention of vascular permeability in retinal diseases characterized by elevated TNF, including diabetic retinopathy.
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Mechanisms of Action of Carbamazepine and Its Derivatives, Oxcarbazepine, BIA 2-093, and BIA 2-024*
TL;DR: The available data indicate that the anticonvulsant efficacy of these AEDs is mainly due to the inhibition of sodium channel activity, which is in line with previous reports on these drugs.
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Inducible nitric oxide synthase isoform is a key mediator of leukostasis and blood-retinal barrier breakdown in diabetic retinopathy.
Ermelindo C. Leal,Ayyakkannu Manivannan,Ken Ichi Hosoya,Tetsuya Terasaki,José Cunha-Vaz,António F. Ambrósio,John V. Forrester +6 more
TL;DR: The results indicate that the iNOS isoform plays a predominant role in leukostasis and BRB breakdown, and the mechanism involves ICAM-1 upregulation and tight junction protein downregulation.
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Contribution of microglia-mediated neuroinflammation to retinal degenerative diseases.
TL;DR: An overview of the roles of microglia-mediated neuroinflammation in major retinal degenerative diseases like glaucoma, age-related macular degeneration, and diabetic retinopathy is given.
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PINK1/PARKIN signalling in neurodegeneration and neuroinflammation.
TL;DR: The role of mitochondrial dysfunction in disorders such as amyotrophic lateral sclerosis, Alzheimer's, Huntington’s and Parkinson's diseases, as well as eye diseases such as age-related macular degeneration and glaucoma, and the causative factors leading to PINK1/PARKIN-mediated neurodegeneration and neuroinflammation are debated.