ReviewInternational journal of molecular sciences2021
The Cardiovascular Phenotype in Fabry Disease: New Findings in the Research Field.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Fabry disease cardiomyopathy: A state-of-the-art review.Progress in cardiovascular diseasesPooled it
- Anderson-Fabry Disease: An Overview of Current Diagnosis, Arrhythmic Risk Stratification, and Therapeutic Strategies.Diagnostics (Basel, Switzerland) · 2025Review
- Inflammation, Oxidative Stress, and Endothelial Dysfunction in the Pathogenesis of Vascular Damage: Unraveling Novel Cardiovascular Risk Factors in Fabry Disease.International journal of molecular sciences · 2024Review
- Clinical staging of Anderson-Fabry cardiomyopathy: An operative proposal.Heart failure reviews · 2024Review
- Fatigue as hallmark of Fabry disease: role of bioenergetic alterations.Frontiers in cardiovascular medicine · 2024Review
- Overexpression of VEGFα as a biomarker of endothelial dysfunction in aortic tissue of α-GAL-Tg/KO mice and its upregulation in the serum of patients with Fabry's disease.Frontiers in cardiovascular medicine · 2024Article
- Endothelial Cell Dysfunction and Hypoxia as Potential Mediators of Pain in Fabry Disease: A Human-Murine Translational Approach.International journal of molecular sciences · 2023Article
- Experimental evidence and clinical implications of Warburg effect in the skeletal muscle of Fabry disease.iScience · 2023Article
- Curcumin Has Beneficial Effects on Lysosomal Alpha-Galactosidase: Potential Implications for the Cure of Fabry Disease.International journal of molecular sciences · 2023Article
- Impact of enzyme replacement therapy and migalastat on left atrial strain and cardiomyopathy in patients with Fabry disease.Frontiers in cardiovascular medicine · 2023Article
- Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease.The Journal of pharmacology and experimental therapeutics · 2023Article
- Pericardial effusion in the course of Fabry disease cardiomyopathy: a case report.European heart journal. Case reports · 2021Article
- Anderson-Fabry Disease: From Endothelial Dysfunction to Emerging Therapies.Advances in pharmacological and pharmaceutical sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fabry disease (FD) is a lysosomal storage disorder, depending on defects in alpha-galactosidase A (GAL) activity. At the clinical level, FD shows a high phenotype variability. Among them, cardiovascular dysfunction is often recurrent or, in some cases, is the sole symptom (cardiac variant) representing the leading cause of death in Fabry patients. The existing therapies, besides specific symptomatic treatments, are mainly based on the restoration of GAL activity. Indeed, mutations of the galactosidase alpha gene (GLA) cause a reduction or lack of GAL activity leading to globotriaosylceramide (Gb3) accumulation in several organs. However, several other mechanisms are involved in FD's development and progression that could become useful targets for therapeutics. This review discusses FD's cardiovascular phenotype and the last findings on molecular mechanisms that accelerate cardiac cell damage.
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What OpenQuestion 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 OpenQuestion graph.