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- W2952783269 abstract "Mitochondrial fatty acid β-oxidation disorders (FAOD) are among the diseases detected by newborn screening in most developed countries. Alterations of mitochondrial functionality are characteristic of these metabolic disorders. However, many questions remain to be clarified, namely how the interplay between the signaling pathways harbored in mitochondria contributes to the disease-related phenotype. Herein, we overview the role of mitochondria on the regulation of cell homeostasis through the production of ROS, mitophagy, apoptosis, and mitochondrial biogenesis. Emphasis is given to the signaling pathways involving MnSOD, sirtuins and PGC-1α, which seem to contribute to FAOD phenotype, namely to multiple acyl-CoA dehydrogenase deficiency (MADD). The association between phenotype and genotype is not straightforward, suggesting that specific molecular mechanisms may contribute to MADD pathogenesis, making MADD an interesting model to better understand this interplay. However, more work needs to be done envisioning the development of novel therapeutic strategies." @default.
- W2952783269 created "2019-06-27" @default.
- W2952783269 creator A5002320088 @default.
- W2952783269 creator A5075468536 @default.
- W2952783269 creator A5076747689 @default.
- W2952783269 date "2019-06-19" @default.
- W2952783269 modified "2023-09-26" @default.
- W2952783269 title "Exploring the contribution of mitochondrial dynamics to multiple acyl-CoA dehydrogenase deficiency-related phenotype" @default.
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- W2952783269 doi "https://doi.org/10.1080/13813455.2019.1628065" @default.
- W2952783269 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31215835" @default.
- W2952783269 hasPublicationYear "2019" @default.
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