Defective chaperone-mediated autophagy in the retinal pigment epithelium of age-related macular degeneration patients

Autophagy is one of the main intracellular recycling systems and its impairment is considered a primary hallmark of the aging process. Defective macroautophagy in the retinal pigment epithelium (RPE) has been described in age-related macular degeneration (AMD), a blindness-causing disease that affec...

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Detalles Bibliográficos
Autores: Jiménez-Loygorri, Juan Ignacio, Shang, Peng, Bayramoglu, Ibrahim, Gómez-Sintes, Raquel, Martín-Segura, Adrián, Ambrosino, Helena, Hoang, Johnson, Díaz, Antonio, Geng, Zhaohui, Gavathiotis, Evripidis, Dutton, James R, Dengjel, Jörn, Cuervo, Ana Maria, Ferrington, Deborah A, Boya, Patricia
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/411389
Acceso en línea:http://hdl.handle.net/10261/411389
https://api.elsevier.com/content/abstract/scopus_id/105020194376
Access Level:acceso abierto
Palabra clave:Age-related Macular degeneration
Chaperone-mediated Autophagy
Oxidative Stress
Proteostasis
Descripción
Sumario:Autophagy is one of the main intracellular recycling systems and its impairment is considered a primary hallmark of the aging process. Defective macroautophagy in the retinal pigment epithelium (RPE) has been described in age-related macular degeneration (AMD), a blindness-causing disease that affects roughly 200 million patients worldwide. The relevance of chaperone-mediated autophagy (CMA), a selective type of autophagy for proteins containing a KFERQ-like motif, in RPE cell biology and homeostasis remains to be elucidated. Here we describe decreased CMA activity in the RPE of AMD patients compared to healthy age-matched controls, along with accumulation of substrate proteins, and in donor-derived iPSC-RPE cells, which we used to further characterize AMD-associated alterations of cellular homeostasis derived from proteotoxicity. Treatment with CA77.1 (CMA activator) restores proteostasis and remodels specific subsets of the proteome in cells from healthy and AMD donors. CA77.1-treated AMD iPSC-RPE display reduced oxidative stress and improved mitochondrial function. These findings may explain the specific vulnerability of the RPE during AMD and shed light on CMA as a new druggable target for this as-of-now incurable disease.