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2015 ; 4
(7
): 1428-47
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Mitochondrial Glutathione in Diabetic Nephropathy
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J Clin Med
2015[Jul]; 4
(7
): 1428-47
PMID26239684
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Although there are many etiologies for diabetic nephropathy (DN), one common
characteristic of all cases involves mitochondrial oxidative stress and
consequent bioenergetic dysfunction. As the predominant low-molecular-weight,
intramitochondrial thiol reductant, the mitochondrial glutathione (mtGSH) pool
plays important roles in how this organelle adapts to the chronic hyperglycemia
and redox imbalances associated with DN. This review will summarize information
about the processes by which this important GSH pool is regulated and how
manipulation of these processes can affect mitochondrial and cellular function in
the renal proximal tubule. Mitochondria in renal proximal tubular (PT) cells do
not appear to synthesize GSH de novo but obtain it by transport from the
cytoplasm. Two inner membrane organic anion carriers, the dicarboxylate carrier
(DIC; Slc25a10) and 2-oxoglutarate carrier (OGC; Slc25a11) are responsible for
this transport. Genetic modulation of DIC or OGC expression in vitro in PT cells
from diabetic rats can alter mitochondrial function and susceptibility of renal
PT cells to oxidants, with overexpression leading to reversion of bioenergetic
conditions to a non-diabetic state and protection of cells from injury. These
findings support the mtGSH carriers as potential therapeutic targets to correct
the underlying metabolic disturbance in DN.
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