Pilar Gonzalez-Cabo

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: It is shown that Saccharomyces cerevisiae frataxin orthologue Yfh1p interacts physically with succinate dehydrogenase complex subunits Sdh1p and Sdh2p of the yeast mitochondrial electron transport chain and also with electron transfer flavoprotein complex ETFalpha and ETFbeta subunits from the electron transfer virus complex.

TL;DR: It is proposed that this C. elegans model may be a useful biological tool for drug screening in Friedreich ataxia by demonstrating synthetic genetic interaction between frh‐1 and mev‐1, the gene encoding the succinate dehydrogenase cytochrome b subunit of complex II in mitochondria, suggesting the respiratory chain might be involved in the pathogenesis of the disease.

TL;DR: To understand the general pathophysiology of the disease and fundamental pathogenic mechanisms such as dying‐back axonopathy, and determine molecular, cellular and tissue therapeutic targets, the effect of frataxin depletion on mitochondrial properties and on specific cell susceptibility in the nervous system and other affected organs needs to be discovered.

TL;DR: The depletion of frataxin did not cause cell death but increased autophagy, which may have a cytoprotective effect against cellular insults such as oxidative stress, and postulate that cellular senescence might be related to a hypoplastic defect in the DRG during neurodevelopment, as suggested by necropsy studies.