ArticleEBioMedicine2017
Paradoxical Inhibition of Glycolysis by Pioglitazone Opposes the Mitochondriopathy Caused by AIF Deficiency.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- BEX1 supports the stemness of hepatoblastoma by facilitating Warburg effect in a PPARγ/PDK1 dependent manner.British journal of cancer · 2023Article
- Pioglitazone Is a Mild Carrier-Dependent Uncoupler of Oxidative Phosphorylation and a Modulator of Mitochondrial Permeability Transition.Pharmaceuticals (Basel, Switzerland) · 2021Article
- PGC1s and Beyond: Disentangling the Complex Regulation of Mitochondrial and Cellular Metabolism.International journal of molecular sciences · 2021Review
- Mitochondrial AIF loss causes metabolic reprogramming, caspase-independent cell death blockade, embryonic lethality, and perinatal hydrocephalus.Molecular metabolism · 2020Article
- Metabolic effects of bezafibrate in mitochondrial disease.EMBO molecular medicine · 2020Observational
- Article
- Physical Exercise and Mitochondrial Disease: Insights From a Mouse Model.Frontiers in neurology · 2019Article
- [Small interfering RNA-mediated monocarboxylate transporter 1 silencing enhances sensitivity of nasopharyngeal carcinoma HNE1/DDP cells to cisplatin-induced apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- An Effective, Versatile, and Inexpensive Device for Oxygen Uptake Measurement.Journal of clinical medicine · 2017Article
- A New Strategy to Treat Mitochondrial Disease Without Improvement of Mitochondrial Function?EBioMedicine · 2017Article
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Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Mice with the hypomorphic AIF-Harlequin mutation exhibit a highly heterogeneous mitochondriopathy that mostly affects respiratory chain complex I, causing a cerebral pathology that resembles that found in patients with AIF loss-of-function mutations. Here we describe that the antidiabetic drug pioglitazone (PIO) can improve the phenotype of a mouse Harlequin (Hq) subgroup, presumably due to an inhibition of glycolysis that causes an increase in blood glucose levels. This glycolysis-inhibitory PIO effect was observed in cultured astrocytes from Hq mice, as well as in human skin fibroblasts from patients with AIF mutation. Glycolysis inhibition by PIO resulted from direct competitive inhibition of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Moreover, GAPDH protein levels were reduced in the cerebellum and in the muscle from Hq mice that exhibited an improved phenotype upon PIO treatment. Altogether, our results suggest that excessive glycolysis participates to the pathogenesis of mitochondriopathies and that pharmacological inhibition of glycolysis may have beneficial effects in this condition.
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