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2017 ; 18
(9
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Thioredoxin 2 Offers Protection against Mitochondrial Oxidative Stress in H9c2
Cells and against Myocardial Hypertrophy Induced by Hyperglycemia
#MMPMID28914755
Li H
; Xu C
; Li Q
; Gao X
; Sugano E
; Tomita H
; Yang L
; Shi S
Int J Mol Sci
2017[Sep]; 18
(9
): ä PMID28914755
show ga
Mitochondrial oxidative stress is thought to be a key contributor towards the
development of diabetic cardiomyopathy. Thioredoxin 2 (Trx2) is a mitochondrial
antioxidant that, along with Trx reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3),
scavenges H?O? and offers protection against oxidative stress. Our previous study
showed that TrxR inhibitors resulted in Trx2 oxidation and increased ROS emission
from mitochondria. In the present study, we observed that TrxR inhibition also
impaired the contractile function of isolated heart. Our studies showed a
decrease in the expression of Trx2 in the high glucose-treated H9c2 cardiac cells
and myocardium of streptozotocin (STZ)-induced diabetic rats. Overexpression of
Trx2 could significantly diminish high glucose-induced mitochondrial oxidative
damage and improved ATP production in cultured H9c2 cells. Notably, Trx2
overexpression could suppress high glucose-induced atrial natriuretic peptide
(ANP) and brain natriuretic peptide (BNP) gene expression. Our studies suggest
that high glucose-induced mitochondrial oxidative damage can be prevented by
elevating Trx2 levels, thereby providing extensive protection to the diabetic
heart.