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Facilitation of Ca 2+ ‐induced opening of the mitochondrial permeability transition pore either by nicotinamide nucleotide transhydrogenase deficiency or statins treatment
Author(s) -
Busanello Estela N.B.,
Figueira Tiago R.,
Marques Ana C.,
Navarro Claudia D.C.,
Oliveira Helena C.F.,
Vercesi Anibal E.
Publication year - 2018
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10949
Subject(s) - mitochondrial permeability transition pore , mitochondrion , nad+ kinase , context (archaeology) , nicotinamide , facilitation , cytosol , chemistry , mptp , pharmacology , microbiology and biotechnology , biochemistry , programmed cell death , biology , disease , medicine , apoptosis , enzyme , neuroscience , paleontology , parkinson's disease
Mitochondrial redox imbalance and high Ca 2+ 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 2+ ‐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.