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AMPK-mediated increase of glycolysis as an adaptive response to oxidative stress in human cells: implication of the cell survival in mitochondrial diseases.

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TLDR
The findings suggest that the increased production of NADPH by AMPK-mediated increase of the glycolytic flux contributes to the adaptation of MERRF skin fibroblasts and H(2)O(2)-treated normal skin fibrablasts to oxidative stress.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2012-02-01 and is currently open access. It has received 162 citations till now. The article focuses on the topics: AMPK & Anaerobic glycolysis.

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Citations
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Metformin in Cancer Treatment and Prevention

TL;DR: The link between metformin and cancer, the potential for met formin in oncology, and limitations of currently available evidence are outlined.
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Cancer as a metabolic disease: implications for novel therapeutics

TL;DR: As each individual is a unique metabolic entity, personalization of metabolic therapy as a broad-based cancer treatment strategy will require fine-tuning to match the therapy to an individual’s unique physiology.
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Oxidative stress response elicited by mitochondrial dysfunction: Implication in the pathophysiology of aging

TL;DR: The positive and integrative roles of mild oxidative stress elicited by mitochondria in the regulation of adaptation, anti-aging and scavenging pathway beyond their roles in the vicious cycle of mitochondrial dysfunction in the aging process are emphasized.
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Interactions between mitochondrial reactive oxygen species and cellular glucose metabolism

TL;DR: It is concluded that more insight in these processes is required to understand why they are (un)able to prevent excessive ROS production during various pathological conditions in humans.
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Role of AMPK-mediated adaptive responses in human cells with mitochondrial dysfunction to oxidative stress.

TL;DR: It is suggested that AMPK may be a potential target for the development of therapeutic agents for the treatment of mitochondrial diseases and a deeper insight into the crosstalk between mitochondria and the nucleus in affected tissue cells from patients with mitochondrial diseases is gained.
References
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Journal ArticleDOI

Mitochondrial diseases in man and mouse.

TL;DR: The essential role of mitochondrial oxidative phosphorylation in cellular energy production, the generation of reactive oxygen species, and the initiation of apoptosis has suggested a number of novel mechanisms for mitochondrial pathology.
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Myoclonic epilepsy and ragged-red fiber disease (MERRF) is associated with a mitochondrial DNA tRNALys mutation

TL;DR: An A to G transition mutation at nucleotide pair 8344 in human mitochondrial DNA has been identified as the cause of MERRF, providing molecular confirmation that some forms of epilepsy are the result of deficiencies in mitochondrial energy production.
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Characterization of the AMP-activated Protein Kinase Kinase from Rat Liver and Identification of Threonine 172 as the Major Site at Which It Phosphorylates AMP-activated Protein Kinase

TL;DR: This finding is consistent with the recent report that the AMP-activated protein kinase kinase can slowly phosphorylate and activate calmodulin-dependentprotein kinase I, at least in vitro.
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The AMP-activated protein kinase pathway – new players upstream and downstream

TL;DR: The AMP-activated protein kinase (AMPK) cascade is a sensor of cellular energy status and regulates food intake and energy expenditure at the whole body level, in particular by mediating the effects of hormones and cytokines such as leptin, adiponectin and ghrelin.
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Phosphorylation and activation of heart PFK-2 by AMPK has a role in the stimulation of glycolysis during ischaemia.

TL;DR: AMPK phosphorylates and activates heart PFK-2 in vitro and in intact cells, and is likely to be involved in the stimulation of heart glycolysis during ischaemia.
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