ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Retinitis Pigmentosa-Associated Gene TRIM49 Regulates ULK1-Mediated Autophagy and Photoreceptor Phagocytosis by the Retinal Pigment Epithelium.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Mapping ophthalmic research on glycosylation and glycation: a PRISMA-compliant bibliometric and co‑citation analysis.Future science OA · 2026Article
- Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Retinitis Pigmentosa-Associated Gene TRIM49 Regulates ULK1-Mediated Autophagy and Photoreceptor Phagocytosis by the Retinal Pigment Epithelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Autophagy is pivotal for cellular homeostasis and photoreceptor outer segment (POS) phagocytosis by the retinal pigment epithelium (RPE) in retinal degenerative diseases, such as age-related macular degeneration and retinitis pigmentosa (RP). Yet, the mechanism of autophagy in the RPE remains largely unknown. RP is an inherited retinal degenerative condition, whose candidate genes provide avenues for dissecting novel autophagy factors. Here, whole exome sequencing of RP patients identified biallelic variants in TRIM49, a primate-specific gene involved in autophagy, as a novel cause of RP. Among human tissues TRIM49 is highly expressed in the RPE. In human RPE cells, deficiency of TRIM49 significantly disturbs cellular homeostasis and impairs the POS phagocytosis. Importantly, suppressed basal autophagy flux is present in TRIM49-depleted RPE cells, whereas enhanced autophagy flux is present in RPE cells overexpressing TRIM49. Variations of TRIM49 after treatment with multiple autophagy modulators indicate that TRIM49 is involved in the initiation of autophagy. TRIM49 interacts with the key regulator of autophagy initiation ULK1. Deficiency of TRIM49 down-regulates and overexpression of TRIM49 up-regulates ULK1 expression. Altogether, these findings identify TRIM49 as a critical regulator of ULK1-mediated autophagy and POS phagocytosis by the RPE, suggesting that RPE autophagy is a potential therapeutic target for retinal degenerative diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.