File:Pathogenesis of Friedreich Ataxia.jpg
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Figure 5
Model of Friedreich's ataxia pathology based on this study. Data presented in this study are consistent with a dysregulation of mitochondrial function, decreased oxidative phosphorylation, increased ROS production, and subsequent mitochondrial and nuclear DNA damage. These factors contribute to decreased signaling and altered DNA transactions, which are likely to result in subsequent loss of protein synthesis and decreased protein degradation, as suggested in the transcription profiling. These alterations may cause tissue damage, altered immune response, and the clinical pathology associated with FRDA.
Reference
<pubmed>20090835</pubmed>| PMC2799513
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Assessment
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Cite this page: Hill, M.A. (2024, March 19) Embryology Pathogenesis of Friedreich Ataxia.jpg. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/File:Pathogenesis_of_Friedreich_Ataxia.jpg
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G
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Date/Time | Thumbnail | Dimensions | User | Comment | |
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current | 12:25, 16 August 2011 | 520 × 380 (30 KB) | Z3329495 (talk | contribs) | Figure 5 Model of Friedreich's ataxia pathology based on this study. Data presented in this study are consistent with a dysregulation of mitochondrial function, decreased oxidative phosphorylation, increased ROS production, and subsequent mitochondrial an | |
12:23, 16 August 2011 | 256 × 256 (9 KB) | Z3329495 (talk | contribs) | Figure 5 Model of Friedreich's ataxia pathology based on this study. Data presented in this study are consistent with a dysregulation of mitochondrial function, decreased oxidative phosphorylation, increased ROS production, and subsequent mitochondrial an |
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