ArticleDiseases (Basel, Switzerland)2016
Integrative Systems Biology Investigation of Fabry Disease.
Article in Diseases (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Identification of Potential Proteins Interacting with α-Galactosidase A to Analyze the Pathogenesis of Fabry Disease.International journal of molecular sciences · 2026Article
- Proteomic analysis unveils Gb3-independent alterations and mitochondrial dysfunction in a glaJournal of translational medicine · 2023Article
- Omics-Based Approaches for the Characterization of Pompe Disease Metabolic Phenotypes.Biology · 2023Review
- Age-related neuroimmune signatures in dorsal root ganglia of a Fabry disease mouse model.Immunity & ageing : I & A · 2023Article
- Integrative OMICS Data-Driven Procedure Using a Derivatized Meta-Analysis Approach.Frontiers in genetics · 2022Article
- Downregulation of orosomucoid 2 acts as a prognostic factor associated with cancer-promoting pathways in liver cancer.World journal of gastroenterology · 2020Article
- Multiple phenotypic domains of Fabry disease and their relevance for establishing genotype- phenotype correlations.The application of clinical genetics · 2019Review
- An integrative systems biology approach for precision medicine in diabetic kidney disease.Diabetes, obesity & metabolism · 2018Review
- Integrative analysis of Multiple Sclerosis using a systems biology approach.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fabry disease (FD) is a rare X-linked recessive genetic disorder caused by a deficient activity of the lysosomal enzyme alpha-galactosidase A (GLA) and is characterised by intra-lysosomal accumulation of globotriaosylceramide (Gb3). We performed a meta-analysis of peer-reviewed publications including high-throughput omics technologies including naïve patients and those undergoing enzyme replacement therapy (ERT). This study describes FD on a systems level using a systems biology approach, in which molecular data sourced from multi-omics studies is extracted from the literature and integrated as a whole in order to reveal the biochemical processes and molecular pathways potentially affected by the dysregulation of differentially expressed molecules. In this way new insights are provided that describe the pathophysiology of this rare disease. Using gene ontology and pathway term clustering, FD displays the involvement of major biological processes such as the acute inflammatory response, regulation of wound healing, extracellular matrix (ECM) remodelling, regulation of peptidase activity, and cellular response to reactive oxygen species (ROS). Differential expression of acute-phase response proteins in the groups of naïve (up-regulation of ORM1, ORM2, ITIH4, SERPINA3 and FGA) and ERT (down-regulation of FGA, ORM1 and ORM2) patients could be potential hallmarks for distinction of these two patient groups.
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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.