ReviewEssays in biochemistry2024
Cardiac arrhythmia in individuals with steroid sulfatase deficiency (X-linked ichthyosis): candidate anatomical and biochemical pathways.
Review in Essays in biochemistry, 2024. 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
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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.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Physiological and Behavioural Characterisation of a Novel Steroid Sulfatase-Deficient Mouse.Genes, brain, and behavior · 2026Article
- Steroid Sulfatase Deficiency: Clinical Manifestations and Psychological Aspects in Light of Current Evidence.Clinical, cosmetic and investigational dermatology · 2026Review
- Association of sarcopenia with atrial fibrillation: protocol for a systematic review and meta-analysis.Systematic reviews · 2025Article
- Sudden Cardiac Arrest in an Adolescent with X-Linked Ichthyosis.Anatolian journal of cardiology · 2025Article
- Monitoring heart rhythms in adult males with X-linked ichthyosis using wearable technology: a feasibility study.Archives of dermatological research · 2025Article
- Sulfation pathways in times of change.Essays in biochemistry · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Circulating steroids, including sex hormones, can affect cardiac development and function. In mammals, steroid sulfatase (STS) is the enzyme solely responsible for cleaving sulfate groups from various steroid molecules, thereby altering their activity and water solubility. Recent studies have indicated that Xp22.31 genetic deletions encompassing STS (associated with the rare dermatological condition X-linked ichthyosis), and common variants within the STS gene, are associated with a markedly elevated risk of cardiac arrhythmias, notably atrial fibrillation/flutter. Here, we consider emerging basic science and clinical findings which implicate structural heart abnormalities (notably septal defects) as a mediator of this heightened risk, and propose candidate cellular and biochemical mechanisms. Finally, we consider how the biological link between STS activity and heart structure/function might be investigated further and the clinical implications of work in this area.
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Registered trials
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