ArticleInternational journal of molecular sciences2023
Endothelial Cell Dysfunction and Hypoxia as Potential Mediators of Pain in Fabry Disease: A Human-Murine Translational Approach.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Fabry Disease: A Focus on the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Lactate metabolic reprogramming and histone lactylation modification in sepsis.International journal of biological sciences · 2025Review
- Human in vitro models for Fabry disease: new paths for unravelling disease mechanisms and therapies.Journal of translational medicine · 2024Review
- Molecular Pathogenesis of Central and Peripheral Nervous System Complications in Anderson-Fabry Disease.International journal of molecular sciences · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Fabry disease (FD) is caused by α-galactosidase A (AGAL) enzyme deficiency, leading to globotriaosylceramide accumulation (Gb3) in several cell types. Pain is one of the pathophysiologically incompletely understood symptoms in FD patients. Previous data suggest an involvement of hypoxia and mitochondriopathy in FD pain development at dorsal root ganglion (DRG) level. Using immunofluorescence and quantitative real-time polymerase chain reaction (qRT PCR), we investigated patient-derived endothelial cells (EC) and DRG tissue of the
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Registered trials
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