ReviewBiomolecules2025
Senior-Loken Syndrome: Ocular Perspectives on Genetics, Pathogenesis, and Management.
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Systemic and Ocular Manifestations of a Ciliopathy: A Case Report of Renal-Retinal Involvement in Senior-Loken Syndrome.Journal of clinical medicine · 2026Article
- From Variant of Uncertain Significance to Likely Pathogenic: Adult-Onset Nephronophthisis Linked to NPHP4 p.T680M.Kidney international reports · 2025Article
- Senior-Løken syndrome with IQCB1/NPHP5 mutation in an adult: a case report.Journal of medical case reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Senior-Loken syndrome (SLSN) is a group of rare autosomal recessive disorders caused by dysfunction of the primary cilium, primarily affecting the kidneys (typically leading to nephronophthisis) and eyes (typically leading to retinal degeneration). Moreover, patients with SLSN may experience additional multisystemic symptoms, such as developmental delay, intellectual disability, ataxia, and nystagmus. To date, eight genes have been demonstrated to cause SLSN, all encoding for proteins involved in the structure and functions of the primary cilium. This places SLSN within an expanding category of diseases known as "ciliopathies". Due to the genetic heterogeneity and significant phenotypic overlap with other ciliopathies, establishing a definitive diagnosis during the initial consultation remains a challenge for clinicians. Furthermore, current research on SLSN-related ciliopathies predominantly focuses on renal involvement, while the ocular manifestations remain insufficiently explored and lack a comprehensive review. Therefore, with the goal of offering practical guidance for clinical practice, this review aims to provide a comprehensive overview of the clinical features, along with an ocular perspective on the molecular mechanisms, genetic underpinnings, and advances in the treatment of SLSN.
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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 OpenQuestion graph.