Increased plasma thioredoxin in patients with acute myocardial infarction

Soejima, Hirofumi; Suefuji, Hisakazu; Miyamoto, Shinzo; Kajiwaram, Ichiro; Kojima, Sunao; Hokamaki, Jun; Sakamoto, Tomohiro; Yoshimura, Michihiro; Nakamura, Hajime; Yodoi, Junji; Ogawa, Hisao

doi:10.1002/clc.4960261208

Cited by 28 publications

(22 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have previously reported that the levels of thioredoxin were elevated in patients with acute coronary syndrome including AMI or unstable angina (25)(26)(27). In the present study we showed that the levels of thioredoxin were significantly higher in patients with CAD than those without CAD.…”

Section: Discussionsupporting

confidence: 65%

Increased Plasma Levels of Thioredoxin in Patients with Glucose Intolerance

et al. 2005

Self Cite

View full text Add to dashboard Cite

Objective The aim of the present study was to determine the effects of glucose intolerance on oxidative stress in patients with coronary artery disease (CAD).Methods The patients were divided into 3 groups, diabetes mellitus (DM), IGT or normal glucose tolerance (NGT) according to the criteria of the American Diabetes Association.Patients The present study consisted of 178 consecutive patients who underwent diagnostic coronary arteriography and a 75-g glucose tolerance test.Results The level of plasma thioredoxin, a marker of oxidative stress was measured in every patient during the fasting state. The levels of plasma thioredoxin were significantly higher in the DM and IGT groups than the NGT group. Furthermore, we found that there was a positive association between thioredoxin levels and glycosylated hemoglobin ( =0.225, p=0.018). In multivariate logistic regression analysis, glucose intolerance (DM or IGT) was only independently associated with the high levels of thioredoxin. The levels of plasma thioredoxin were significantly higher in the CAD group compared to the non-CAD group. In multivariate logistic regression analysis, high levels of thioredoxin, male, age and hypertension were independently associated with the presence of CAD.Conclusion Glucose intolerance was associated with the high levels of thioredoxin. High levels of thioredoxin were related to the presence of CAD. The measurement of thioredoxin as the marker of oxidative stress may be useful for monitoring the development of the cardiovascular diseases.

show abstract

Section: Discussionsupporting

confidence: 65%

Increased Plasma Levels of Thioredoxin in Patients with Glucose Intolerance

et al. 2005

Self Cite

View full text Add to dashboard Cite

show abstract

“…In the clinical setting, we have previously investigated the correlation between ROS generation and coronary heart disease. [32][33][34][35] Our previous studies have demonstrated that oxidative stress markers, including plasma thioredoxin levels, urinary biopyrrins and 8-hydroxy-2'-deoxyguanosine excretion, were elevated in patients with AMI. We have previously reported that increased ROS may predict subsequent cardiovascular events; however, it was still unknown whether edaravone administration reduces ROS generation during the clinical course of AMI in humans.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Efficacy of Edaravone in Patients With Acute Myocardial Infarction

Tsujita

Shimomura

Kaikita

et al. 2006

Circ J

Self Cite

View full text Add to dashboard Cite

yocardial reperfusion is necessary for the salvage and recovery of the ischemic myocardium. Early reperfusion therapy has improved the clinical outcomes of patients with acute myocardial infarction (AMI), but these benefits are limited in some patients by reperfusion injuries. 1 There is now increasing evidence that reactive oxygen species (ROS) lead to reperfusion injuries in the ischemic myocardium and that they are related to subsequent left ventricular (LV) dysfunction. 2,3 Recent investigations have shown that increased vascular oxidative stress predicts the risk of cardiovascular events in patients with coronary artery disease. 4 Various different radical scavengers and antioxidants have been shown to effectively reduce reperfusion injury in experimental models. 5,6 In these ischemia-reperfusion models, it was demonstrated that radical scavengers such as superoxide dismutase and vitamin E analog reduced infarct size by limiting reperfusion-induced oxidative stress and by attenuating the inflammatory response. On the basis of this established scientific rationale, several randomized controlled trials were designed to prove or disprove the causative effects for antioxidant supplements. 7-10 Unfortunately, results of these studies on antioxidants and cardiovascular event risks have been disappointing, especially in regards to the studies investigating primary prevention. Namely, each study has several limitations to test therapeutic agents in clinical practice, mainly because of their low accessibility to tissue or rapid clearance from the body. 11,12 In contrast, edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), has a low molecular weight (174.20 kD), is lipophilic, and is readily accessible to tissue. 13,14 Edaravone has the ability to scavenge toxic free radicals; moreover, it has been shown to inhibit vascular endothelial cell injury and to inhibit the aggravation of brain edema caused by free radical-induced lipid peroxidation. 15 Recently, edaravone has been officially approved for the treatment of acute ischemic stroke in Japan. 16 Previous experimental studies have reported that the administration of edaravone just before reperfusion reduced reperfusion injuries and myocardial damage in myocardial ischemia-reperfusion animal models. 17,18 Edaravone has been shown to attenuate pressure overload-induced LV hypertrophy via its antioxidant function according to a recent report. 19 With these effects, edaravone has been recognized as both a potent cardioprotective and a cytoprotective agent. We have recently demonstrated that the administration of edaravone just prior to myocardial reperfusion attenuated both enzymatic infarct size and reperfusion arrhythmia in patients with AMI; 20 however, its effects on long-term clinical outcomes in AMI patients have not yet been clarified. The purpose of the present study was to clarify the efficacy of edaravone on the long-term prognosis in patients with AMI. Long-Term Efficacy of Edaravone in Patients With Acute Myocardial InfarctionKenichi Tsujita, MD; Hideki Shimo...

show abstract

“…Plasma Trx-1 levels are elevated in patients with unstable angina, spastic angina, and acute myocardial infraction compared with those in stable exertional angina and chest-pain syndrome (61,120,165). Elevated Trx-1 levels in acute myocardial infraction are associated with hyperaggregation of platelet, which indicates further risk as well as pathogenesis of ischemic heart diseases (123).…”

Section: Thioredoxin-glutaredoxin and Related Molecules As Biomarkersmentioning

confidence: 99%

“…The mitochondrial protein SP-22 exerts its cardioprotective effect in rat heart as an antioxidant molecule (5). However, the higher expression level of serum or plasma Trx-1 is indicative of a risk factor for the patients with acute myocardial infarction (AMI), in which Trx-1 could enhance platelet aggregability and reduce the left ventricular ejection fraction (123,165).…”

Section: Ischemic Heart Diseasesmentioning

confidence: 99%

Redox Regulation of Cell Survival by the Thioredoxin Superfamily: An Implication of Redox Gene Therapy in the Heart

Ahsan

Lekli

Ray

et al. 2009

Antioxidants & Redox Signaling

Self Cite

117

View full text Add to dashboard Cite

Reactive oxygen species (ROS) are the key mediators of pathogenesis in cardiovascular diseases. Members of the thioredoxin superfamily take an active part in scavenging reactive oxygen species, thus playing an essential role in maintaining the intracellular redox status. The alteration in the expression levels of thioredoxin family members and related molecules constitute effective biomarkers in various diseases, including cardiovascular complications that involve oxidative stress. Thioredoxin, glutaredoxin, peroxiredoxin, and glutathione peroxidase, along with their isoforms, are involved in interaction with the members of metabolic and signaling pathways, thus making them attractive targets for clinical intervention. Studies with cells and transgenic animals have supported this notion and raised the hope for possible gene therapy as modern genetic medicine. Of all the molecules, thioredoxins, glutaredoxins, and peroxiredoxins are emphasized, because a growing body of evidence reveals their essential and regulatory role in several steps of redox regulation. In this review, we discuss some pertinent observations regarding their distribution, structure, functions, and interactions with the several survival-and death-signaling pathways, especially in the myocardium. Antioxid. Redox Signal. 11, 2741-2758.

show abstract

Increased plasma thioredoxin in patients with acute myocardial infarction

Cited by 28 publications

References 22 publications

Increased Plasma Levels of Thioredoxin in Patients with Glucose Intolerance

Increased Plasma Levels of Thioredoxin in Patients with Glucose Intolerance

Long-Term Efficacy of Edaravone in Patients With Acute Myocardial Infarction

Redox Regulation of Cell Survival by the Thioredoxin Superfamily: An Implication of Redox Gene Therapy in the Heart

Contact Info

Product

Resources

About