ReviewBiomolecules2025
Alternative Splicing Dysregulation in Retinitis Pigmentosa: Pathogenic Mechanisms and Therapeutic Opportunities.
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Lateral Geniculate Nucleus Volume Assessment Using Linear Mixed Model in Moderate and Advanced Retinitis Pigmentosa.Journal of clinical medicine · 2026Article
- Müller Glia-Exclusive CLRN1 Expression Drives Non-Cell-Autonomous Photoreceptor Degeneration in Usher Syndrome Type 3A.Investigative ophthalmology & visual science · 2026Article
- Inferring genetic associations of programmed cell death genes with retinitis pigmentosa through multimodal Mendelian randomization.Molecular medicine (Cambridge, Mass.) · 2026Article
- Transferrin receptor 1: an emerging therapeutic target in cancer beyond iron metabolism.Cancer cell international · 2026Review
- Disrupting SRSF10-dependent BCAT2 exon skipping reprograms tumor-associated macrophages and enhances anti-PD-1 efficacy in gastric cancer.Cell death & disease · 2026Article
- From Genetic Diagnosis to Therapeutic Implementation in Retinal Diseases: Translational Advances and Persistent Bottlenecks.Biomedicines · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Retinitis pigmentosa (RP) represents a genetically heterogeneous group of inherited retinal dystrophies characterized by progressive photoreceptor degeneration and irreversible vision loss. Among the diverse pathogenic mechanisms, dysregulation of alternative splicing has emerged as a pivotal driver, particularly in RP cases caused by mutations in splicing factors or cis-regulatory elements. Alternative splicing governs transcript diversity and fine-tunes gene expression, with more than 95% of human multi-exon genes undergoing this process. Disruption of precise splicing patterns in the retina-an organ with exceptionally high transcriptional complexity-leads to widespread mis-splicing of photoreceptor-specific genes, triggering retinal dysfunction and cell death. This review synthesizes current understanding of alternative splicing-related mechanisms in RP, integrating molecular insights from splicing-factor mutations, retina-specific splice isoforms, and their downstream cellular consequences. We also evaluate therapeutic strategies targeting splicing dysregulation, including antisense oligonucleotides (ASOs), modified U1 snRNA, spliceosome-mediated RNA trans-splicing (SMaRT), and genome editing, emphasizing translational potential and clinical challenges. Finally, we highlight key research gaps and propose future directions for splicing-centered precision medicine in RP.
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What Socratic holds
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.