Facilitation of Ca 2+ -induced opening of the mitochondrial permeability transition pore either by nicotinamide nucleotide transhydrogenase deficiency or statins treatment

Mitochondrial redox imbalance and high Ca uptake induce the opening of the permeability transition pore (PTP) that leads to disruption of energy-linked mitochondrial functions and triggers cell death in many disease states. In this review, we discuss the major results from our studies investigating...

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Bibliographic Details
Published in:Cell biology international 2018-06, Vol.42 (6), p.742-746
Main Authors: Busanello, Estela N B, Figueira, Tiago R, Marques, Ana C, Navarro, Claudia D C, Oliveira, Helena C F, Vercesi, Anibal E
Format: Article
Language:English
Subjects:
Animals
Calcium - metabolism
Diet, High-Fat
Fatty Liver - drug therapy
Fatty Liver - etiology
Fatty Liver - veterinary
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondrial Membrane Transport Proteins - metabolism
NADP Transhydrogenases - genetics
NADP Transhydrogenases - metabolism
Permeability - drug effects
Ubiquinone - analogs & derivatives
Ubiquinone - chemistry
Ubiquinone - metabolism
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Summary:Mitochondrial redox imbalance and high Ca uptake induce the opening of the permeability transition pore (PTP) that leads to disruption of energy-linked mitochondrial functions and triggers cell death in many disease states. In this review, we discuss the major results from our studies investigating the consequences of NAD(P)-transhydrogenase (NNT) deficiency, and of statins treatment for mitochondrial functions and susceptibility to Ca -induced PTP. We highlight the aggravation of high fat diet-induced fatty liver disease in the context of NNT deficiency and the role of antioxidants in the prevention of statins toxicity to mitochondria.
ISSN:1065-6995
1095-8355
DOI:10.1002/cbin.10949