Thioredoxin-1 Attenuates Ventricular and Mitochondrial Postischemic Dysfunction in the Stunned Myocardium of Transgenic Mice

Abstract

These results strongly suggest that Trx1 ameliorates the myocardial effects of I/R by improving the free radical-mediated damage in cardiac and mitochondrial function, opening the possibility of new therapeutic strategies in coronary artery disease. Antioxid. Redox Signal. 25, 78-88.

Nuclear Factor (Erythroid-Derived 2)-Like 2 and Thioredoxin-1 in Atherosclerosis and Ischemia/Reperfusion Injury in the Heart

“…High levels of ROS resulted in loss of Trx-1, which was demonstrated by Perez et al, 120 min after reperfusion. Loss of Trx-1 then leads to an ''over''-adaptive response, which explains the opposite finding of an increase of Trx-1 24 h after the reperfusion phase (80). Analyzing Trx-1 levels in cardiac tissue biopsies collected from cardiopulmonary bypass surgeries revealed an increase of Trx-1 in patients who were preconditioned by four cycles of 5 min upper arm ischemia followed by a 5 min reperfusion phase (113).…”

Thioredoxin 1 is upregulated in the bone and bone marrow following experimental myocardial infarction: evidence for a remote organ response

“…The understanding of post-ischemic events remains critical for the development of novel therapeutic approaches in ischemia-reperfusion pathologies. Although redox proteins in IR have been intensely studied, most of the research has focused on the primarily affected organ as the main injured tissue (Shau et al 2000;Matsushima et al 2006;Godoy et al 2011b;Romero et al 2015;Perez et al 2016). Remote organ responses of redox regulatory proteins after IR, on the other side, represent an unexplored but yet exciting area of research that may broaden our understanding of redox regulation in the multi-systemic conditions encountered in vivo.…”

Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review

“…Decreased apoptosis levels were observed for PRDX6 in vitro in SCOV-3 cell lines treated with cisplatin [ 169 ], for PRDX5 in human tendon fibroblasts treated with H 2 O 2 [ 161 ], and in HT29 cells treated with shikonin [ 166 ], for TRX1 in WEHI7.2 lymphoma cells treated with H 2 O 2 [ 220 ], in in vivo studies on transgenic mice that were treated with methamphetamine [ 214 ], and for SRXN1 in retinal ganglion cells (RGC) of mice treated with high glucose concentrations [ 229 ]. Among the positive effects of overexpression, for PRDX5 , researchers have shown decreased DNA damage in hamster cell cultures CHO-K1 exposed to H 2 O 2 and tert-butylhydroperoxide (tBHP) [ 162 ] as well as for TRX1 in the mitochondria of transgenic mice Trx1-Tg in vivo in sepsis-induced myocardial dysfunction and sham surgery [ 216 , 217 ]. Increased expression of TRX1 in mice in vivo [ 217 ] and ex vivo [ 218 ] decreased the negative consequences of ischemia for the cardiovascular system.…”

“…Among the positive effects of overexpression, for PRDX5 , researchers have shown decreased DNA damage in hamster cell cultures CHO-K1 exposed to H 2 O 2 and tert-butylhydroperoxide (tBHP) [ 162 ] as well as for TRX1 in the mitochondria of transgenic mice Trx1-Tg in vivo in sepsis-induced myocardial dysfunction and sham surgery [ 216 , 217 ]. Increased expression of TRX1 in mice in vivo [ 217 ] and ex vivo [ 218 ] decreased the negative consequences of ischemia for the cardiovascular system. Using oxygen–glucose deprivation/reoxygenation in in vitro experiments showed that the ability of PON2 to enhance glucose transport and to suppress oxidative stress and apoptosis is potentially a good set of properties to prevent cerebral ischemia-reperfusion injury [ 143 ].…”

“…Increased resistance: H 2 O 2 [212,220,224], daunomycin [213], MPP+ [215], menadione, 1-chloro-2,4-dinitrobenzene [71], arsenic trioxide [222,223] Unchanged resistance: dexamethasone, doxorubicin, etoposide [220], auranofin, juglone [71] in vivo Increased resistance: methamphetamine [214,221], sepsis-induced myocardial dysfunction, sham surgery [216], ischemia [217,225], ex vivo ischemia [218], adriamycin [219] TXNL1 in vitro Decreased resistance: cisplatin [226] TXNRD1 in vitro Increased resistance: X-ray [227], H 2 O 2 [224] Cases of spontaneous gene overexpression in tumors resistant to particular therapy types were also reviewed, but only in such cases where the abolition of overexpression of a particular gene led to the abolition of the changed phenotype.…”