ArticleInternational journal of molecular sciences2020
Underestimated Aspect of Mucopolysaccharidosis Pathogenesis: Global Changes in Cellular Processes Revealed by Transcriptomic Studies.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- TFEB, FOXO3 and TLR4 in resveratrol-induced autophagy in a mucopolysaccharidosis IIIB mouse model.Experimental & molecular medicine · 2026Article
- Mitochondrial morphology and mtDNA content in fibroblasts from patients with different types of mucopolysaccharidosis.Acta biochimica Polonica · 2026Article
- Advances in mucopolysaccharidosis research: the impact of mass spectrometry-based approaches.Clinical proteomics · 2025Review
- Mucopolysaccharidoses-What Clinicians Need to Know: A Clinical, Biochemical, and Molecular Overview.Biomolecules · 2025Review
- A Drosophila model of mucopolysaccharidosis IIIB.Genetics · 2025Article
- The Role of Gene Expression Dysregulation in the Pathogenesis of Mucopolysaccharidosis: A Comparative Analysis of Shared and Specific Molecular Markers in Neuronopathic and Non-Neuronopathic Types of the Disease.International journal of molecular sciences · 2024Article
- Cellular Organelle-Related Transcriptomic Profile Abnormalities in Neuronopathic Types of Mucopolysaccharidosis: A Comparison with Other Neurodegenerative Diseases.Current issues in molecular biology · 2024Article
- Metabolic rewiring and autophagy inhibition correct lysosomal storage disease in mucopolysaccharidosis IIIB.iScience · 2024Article
- Modeling skeletal dysplasia in Hurler syndrome using patient-derived bone marrow osteoprogenitor cells.JCI insight · 2024Article
- Evidence of epigenetic landscape shifts in mucopolysaccharidosis IIIB and IVA.Scientific reports · 2024Article
- Mucopolysaccharidosis IVA: Current Disease Models and Drawbacks.International journal of molecular sciences · 2023Review
- Enhanced Efficiency of the Basal and Induced Apoptosis Process in Mucopolysaccharidosis IVA and IVB Human Fibroblasts.International journal of molecular sciences · 2023Article
- Dysregulation of genes coding for proteins involved in metabolic processes in mucopolysaccharidoses, evidenced by a transcriptomic approach.Metabolic brain disease · 2023Article
- Article
- Tubulin Cytoskeleton in Neurodegenerative Diseases-not Only Primary Tubulinopathies.Cellular and molecular neurobiology · 2023Review
- Transcriptomic Approaches in Studies on and Applications of Chimeric Antigen Receptor T Cells.Biomedicines · 2023Review
- Decreased Levels of Chaperones in Mucopolysaccharidoses and Their Elevation as a Putative Auxiliary Therapeutic Approach.Pharmaceutics · 2023Article
- Roles of the Oxytocin Receptor (OXTR) in Human Diseases.International journal of molecular sciences · 2023Review
- Article
- Activities of (Poly)phenolic Antioxidants and Other Natural Autophagy Modulators in the Treatment of Sanfilippo Disease: Remarkable Efficacy of Resveratrol in Cellular and Animal Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
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8 authors at 1 institution in 1 country.
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Abstract
Mucopolysaccharidoses (MPS), a group of inherited metabolic disorders caused by deficiency in enzymes involved in degradation of glycosaminoglycans (GAGs), are examples (and models) of monogenic diseases. Accumulation of undegraded GAGs in lysosomes was supposed to be the major cause of MPS symptoms; however, their complexity and variability between particular types of the disease can be hardly explained by such a simple storage mechanism. Here we show that transcriptomic (RNA-seq) analysis of the material derived from fibroblasts of patients suffering from all types and subtypes of MPS, supported by RT-qPCR results, revealed surprisingly large changes in expression of genes involved in various cellular processes, indicating complex mechanisms of MPS. Although each MPS type and subtype was characterized by specific changes in gene expression profile, there were genes with significantly changed expression relative to wild-type cells that could be classified as common for various MPS types, suggesting similar disturbances in cellular processes. Therefore, both common features of all MPS types, and differences between them, might be potentially explained on the basis of changes in certain cellular processes arising from disturbed regulations of genes' expression. These results may shed a new light on the mechanisms of genetic diseases, indicating how a single mutation can result in complex pathomechanism, due to perturbations in the network of cellular reactions. Moreover, they should be considered in studies on development of novel therapies, suggesting also why currently available treatment methods fail to correct all/most symptoms of MPS. We propose a hypothesis that disturbances in some cellular processes cannot be corrected by simple reduction of GAG levels; thus, combined therapies are necessary which may require improvement of these processes.
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