ArticleBiochemistry and biophysics reports2022
Oxidized low-density lipoprotein causes ribosome reduction and inhibition of protein synthesis in retinal pigment epithelial cells.
Article in Biochemistry and biophysics reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Neuronal death and accumulation of lipid droplets and glycogen granules within retinal pigment epithelium under the influence of mTOR and autophagy.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Proteasome and Ribosome Ubiquitination in Retinal Pigment Epithelial (RPE) Cells in Response to Oxidized Low-Density Lipoprotein (OxLDL).Biomedicines · 2025Article
- Modulation of mTOR Within Retinal Pigment Epithelium Affects Cell Viability and Mitochondrial Pathology.International journal of molecular sciences · 2025Article
- Article
- Retinal Autophagy for Sustaining Retinal Integrity as a Proof of Concept for Age-Related Macular Degeneration.International journal of molecular sciences · 2025Review
- Low-Density Lipoproteins Increase Proliferation, Invasion, and Chemoresistance via an Exosome Autocrine Mechanism in MDA-MB-231 Chemoresistant Cells.Biomedicines · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal pigment epithelium (RPE) are specialized multifunctional cells indispensable for maintenance of vision. Dysfunction and death of the RPE cells is implicated in the genesis and progression of age-related macular degeneration (AMD). Oxidative stress and resulting cellular damage plays a critical mechanistic role in AMD pathogenesis. Oxidized low-density lipoprotein (oxLDL), derived from LDL in a pro-oxidative environment, is found adjacent to the RPE as part of drusen, extracellular deposits that are a characteristic clinical feature of AMD. OxLDL is cytotoxic and oxLDL-induced oxidative damage may contribute to functional impairment of the RPE. Therefore, knowledge of how the RPE respond to oxLDL exposure is important to understand the mechanisms underlying RPE dysfunction and death associated with AMD. The objective of this study was to characterize alterations in the RPE proteome triggered by exposure to non-cytotoxic levels of oxLDL. Protein identification and quantification were performed with a high -resolution LC-MS/MS-based proteomics workflow. In total, out of the
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