Mitochondrial dysfunction induces oxidative stress and an impaired ubiquitin proteasome system to trigger the pathogenesis of Frontal Fibrosing Alopecia (FFA)
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ABSTRACT: Mitochondrial dysfunction is implicated in myriad diseases. However, there is no single platform that facilitates mapping of mitochondrial pathways and processes essential for health and those that are defective in disease. Here, we manually curated 1008 mitochondrial proteins to create a database of 31 mitochondrial pathways and processes and named the database as ‘MitoGyan’. ‘Gyan’ in Sanskrit means knowledge. We also developed a mitochondria associated metabolic pathways visualization tool called MitoCyc within HumanCyc. Using these novel resources and an integrated ‘Omics’ approach, we demonstrate that mitochondrial dysfunction occurs early in a rare, inflammatory hair disease called Frontal Fibrosing Alopecia (FFA). Transmission electron microscopy and mass spectrometry show morphological and functional changes in the mitochondria of FFA hair follicles. Our data suggests that mitochondrial dysfunction induces oxidative stress and an impairment of the ubiquitin proteasome system (UPS) in FFA. We propose that mitochondria-targeted antioxidants provide a new therapeutic strategy for FFA. Microarray analyses of FFA was undertaken to decipher pathophysiological pathways of FFA leading to disease intitiation and progression
ORGANISM(S): Homo sapiens
PROVIDER: GSE58934 | GEO | 2021/12/21
REPOSITORIES: GEO
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