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Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy

PURPOSE: The Slc4a11 knock out (KO) mouse model recapitulates the human disease phenotype associated with congenital hereditary endothelial dystrophy (CHED). Increased mitochondrial reactive oxygen species (ROS) in the Slc4a11 KO mouse model is a major cause of edema and endothelial cell loss. Here,...

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Detalles Bibliográficos
Autores principales: Shyam, Rajalekshmy, Ogando, Diego G., Choi, Moonjung, Liton, Paloma B., Bonanno, Joseph A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Association for Research in Vision and Ophthalmology 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8458782/
https://www.ncbi.nlm.nih.gov/pubmed/34533563
http://dx.doi.org/10.1167/iovs.62.12.15