Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Kishimoto, Chiharu; Shioji, Kosei; Nakamura, Hajime; Nakayama, Yasushi; Yodoi, Junji; Sasayama, Shígetake

doi:10.1253/jcj.65.491

Cited by 81 publications

(52 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…15 We documented that the elevation of serum TRX1 levels correlated with the severity of New York Heart Association functional class and negatively correlated with left ventricular ejection fractions in patients with heart diseases. 19 These findings suggest that TRX1 per se and the redox system modulated by TRX1 have a important role in the cellular defense against oxidative stress in cardiomyocytes as well as in other cell types, such as neurons 11 and hepatocytes. 20 Most studies support the view that both an increase in oxidative stress and a decrease in antioxidants play an important role in the pathogenesis of ADR cardiomyopathy.…”

Section: Discussionmentioning

confidence: 95%

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

et al. 2002

Self Cite

View full text Add to dashboard Cite

Background-Adriamycin (ADR) is an anticancer drug known to cause severe cardiac toxicity by generating free radicals.We investigated the role of a redox-regulating molecule, thioredoxin-1 (TRX1), in ADR-induced cardiotoxicity. Methods and Results-The in vitro study showed that TRX1 was dose-dependently increased concomitant with the formation of hydroxyl radicals in ADR-treated neonatal rat cardiomyocytes. Lactate dehydrogenase-releasing assay showed that treatment with recombinant human TRX1 suppressed cardiomyocyte injury in ADR-treated cardiomyocytes. To examine the biological significance of TRX1 in vivo, we used transgenic mice expressing increased levels of human TRX1 (TRX1-TG mice). Electron microscopy revealed that mitochondria, myofibrils, and other cellular details were much better maintained in ADR-treated TRX1-TG mice than in ADR-treated nontransgenic (WT) mice. The increase in the protein carbonyl content, a marker of cellular protein oxidation, was suppressed in ADR-treated TRX1-TG mice compared with ADR-treated WT mice. The formation of hydroxyl radicals in ADR-treated heart homogenates of TRX1-TG mice was decreased compared with WT mice. For the survival study, all WT mice treated with ADR died within 6 weeks, but 5 of 6 TRX1-TG mice treated with ADR survived Ͼ8 weeks. Conclusions-TRX1 is upregulated by intracellular oxidative stress generated by ADR. TRX1 has a protective role against ADR-induced cardiotoxicity by reducing oxidative stress.

show abstract

Section: Discussionmentioning

confidence: 95%

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

et al. 2002

Self Cite

View full text Add to dashboard Cite

show abstract

“…Serum concentrations have been reported to be elevated to approximately 30 ng/ml in patients with congestive heart failure, more than 100 ng/ml in a patient with fulminant myocarditis and also 64±44 ng/ml in patients with coronary spastic angina in the active stage. 21,22,24 The present data on serum TRX concentrations, combined with its known properties, suggest that the serum concentration of TRX can be used as a generalized marker for oxidative stress and redox-equilibrium, although the correlation between serum TRX concentrations and the other markers for oxidative stress remains to be clarified and needs to be examined.…”

Section: Serum Trx Concentration As a Measure Of Oxidative Stressmentioning

confidence: 86%

Serum Thioredoxin and .ALPHA.-Tocopherol Concentrations in Patients With Major Risk Factors

Miwa

Kishimoto²,

Nakamura

et al. 2005

Circ J

Self Cite

View full text Add to dashboard Cite

“…The elevation of serum thioredoxin levels in patients with heart failure has been reported. 6 Although the precise mechanism of thioredoxin secretion is still not clarified, plasma levels of human thioredoxin are the response against oxidative stress. 7 There is a possibility that plasma thioredoxin levels were elevated by the inflammatory response against the oxidative stress in patients with AMI in the present study.…”

Section: Discussionmentioning

confidence: 99%

Increased plasma thioredoxin in patients with acute myocardial infarction

Soejima

Suefuji

Miyamoto

et al. 2003

Clinical Cardiology

Self Cite

View full text Add to dashboard Cite

SummaryBackground and hypothesis: Thioredoxin is an important biomarker for oxidative stress. We investigated whether thioredoxin levels were elevated in patients with acute myocardial infarction (AMI) and were associated with the results of coronary reperfusion.Methods: The present study determined plasma thioredoxin levels in 51 patients with AMI, 30 patients with stable exertional angina (SEA), and 30 patients with chest pain syndrome (CPS). Plasma sampling was performed on admission, at 12 h, 1 week, 2 weeks, and 4 weeks in patients with AMI, and after admission in patients with SEA and CPS.Results: Plasma thioredoxin levels on admission were higher in patients with AMI than in those with SEA and CPS. Plasma thioredoxin levels in patients with AMI were decreased in 12 h without further change thereafter. However, thioredoxin levels in patients with AMI remained higher than in those with SEA. In multivariate analysis, higher levels of thioredoxin on admission were a risk factor for failure in emergent reperfusion therapy in patients with AMI independent of other factors.

show abstract

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Cited by 81 publications

References 25 publications

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

Serum Thioredoxin and .ALPHA.-Tocopherol Concentrations in Patients With Major Risk Factors

Increased plasma thioredoxin in patients with acute myocardial infarction

Contact Info

Product

Resources

About