Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An increase in oxidative stress is thought to be involved in the progression of heart disease, but the serum level of thioredoxin (TRX), which regulates the cellular redox state, has not been investigated in patients with heart diseases. The present study determined serum TRX levels with a sandwich enzyme-linked immunosorbent assay in a total of 39 patients with dilated cardiomyopathy (DCM) (n=5), acute coronary syndrome (ACS) (n=7) or stable angina (n=18), including effort angina (n=7) and vasospastic angina (n=11), and in control subjects (n=7). The serum TRX level in patients with New York Heart Association (NYHA) functional classes III and IV (n=8, 33.3+/-8.6 ng/ml) was significantly higher than in the control subjects (n=7, 14.0+/-4.6 ng/ml). In addition, the serum TRX levels correlated positively with the severity of NYHA class, and negatively with the left ventricular ejection fraction. The serum TRX levels were elevated in patients with ACS and DCM compared with the controls. These results indicate a possible association between TRX concentration and the severity of heart failure.
 ...
PMID:Serum thioredoxin (TRX) levels in patients with heart failure. 1140 28

To determine whether plasma levels of thioredoxin are associated with coronary spasm, we measured the plasma levels of thioredoxin in 170 patients who had <25% organic stenosis in coronary arteriography. According to the results of cardiac catheterization, we divided the patients into two groups: a coronary spastic angina group (n=84) and a chest pain syndrome group (n=86). The plasma levels of thioredoxin were significantly higher in the coronary spastic angina group than in the chest pain syndrome group (40.7 +/- 4.1 versus 18.2 +/- 1.1 ng/ml, p<0.0001). Furthermore, the increased plasma levels of thioredoxin were associated with high disease activity indicated by the frequency of angina attacks (p=0.0004). In multiple logistic regression analysis, the higher levels of thioredoxin [relative risk 14.8, 95% confidence interval (5.13-42.9), p<0.0001] and current smoking [relative risk 3.39, 95% confidence interval (1.31-8.75), p=0.012] were significant and independent variables associated with coronary spasm. We demonstrated that the plasma levels of thioredoxin were increased in the coronary spastic angina group, and increased levels of thioredoxin were associated with high disease activity. The plasma levels of thioredoxin and current smoking were risk factors for coronary spastic angina, and they were independent from other traditional risk factors.
 ...
PMID:Increased plasma levels of thioredoxin in patients with coronary spastic angina. 1471 37

The present study investigated the expression of thioredoxin (TRX), an important anti-oxidative protein, and its relationship to plaque instability in atherectomy specimens from 43 and 42 patients with stable (SAP) and unstable (UAP) angina pectoris, respectively. We histologically assessed thrombus formation, cellular elements, localization of TRX and of oxidized low density lipoprotein (ox-LDL), intraplaque hemorrhage, and transition metal iron (Fe(2+), Fe(3+)) deposition in these specimens. The clinical characteristics of the two groups did not differ except for aspirin administration. The incidence of thrombus formation was more frequent (P=0.005) and immunopositive areas of macrophage, TRX and ox-LDL were significantly larger in patients with UAP than SAP (P<0.001, each). Macrophages were mainly immunoreactive for TRX and ox-LDL. Intraplaque hemorrhage evaluated by glycophorin A immunoreactivity and Fe(2+)/Fe(3+) deposition was also more obvious in lesions from patients with UAP than SAP (P<0.001, each). Additionally, immunopositive areas of TRX and ox-LDL positively correlated with Fe(2+)/Fe(3+) deposition and were also associated with thrombus formation. Although the underlying mechanisms remain unknown, TRX was up-regulated in response to increased oxidative stress and associated with intraplaque hemorrhage of coronary culprit lesions, and thus might be a potent marker of plaque instability.
 ...
PMID:Thioredoxin in coronary culprit lesions: possible relationship to oxidative stress and intraplaque hemorrhage. 1842 Feb 12

Carvedilol is a third-generation beta-blocker, with the S-enantiomer being more active than the R-enantiomer. Clinically, it has been used in the treatment of hypertension, congestive heart failure and angina pectoris. Each enantiomer of Carvedilol exhibits differential pharmacological effects. However, the cellular effects of individual enantiomer are not well understood. To gain insights into how each enantiomer affects cells, we analysed differential protein expression levels in vascular smooth muscle cells (A7r5) incubated separately with S- and R-Carvedilol by iTRAQ-coupled 2-D LC-MS/MS approach. Thirteen proteins were identified with statistically significant changes in cells incubated with S-Carvedilol, while the changes of most proteins incubated with R-Carvedilol were less significant. Among these proteins, actin in aortic smooth muscle (ACTA2), calmodulin, S100-A6, S100-A10, S100-A11, thioredoxin, lactadherin and heat-shock protein 105 kDa were found to be closely relevant with the clinical effects of Carvedilol. Furthermore, the changes in protein levels were validated by Western blot. Our findings thus provided molecular evidence on a comprehensive protein profile on Carvedilol-cell interaction, which may shed new light in molecular events underlying Carvedilol treatment.
 ...
PMID:Proteomic profiling of cellular responses to Carvedilol enantiomers in vascular smooth muscle cells by iTRAQ-coupled 2-D LC-MS/MS. 2040 66

The anti-angina agent nicorandil has been reported to be beneficial even in patients who have angina with diabetes. However, the mechanism underlying the effect of nicorandil in patients with diabetes remains to be elucidated. In this study, the protective effect of nicorandil on thioredoxin (TRX) protein was investigated, as TRX is a multifunctional endogenous redox regulator that protects cells against various types of cellular and tissue stress. This study was conducted to examine whether nicorandil induces the expression of TRX for the protection against diabetic damage in the vascular tissue of rats. Diabetes was induced in rats by intraperitoneal injection of streptozotocin (STZ) (fasting glucose levels in STZ-induced rats were >14 mmol/l). Diabetic rats were divided into a diabetic control and a nicorandil-treated group. Nicorandil was administered at a dosage of 15 mg/kg/day by gavage feeding. After five weeks of nicorandil administration, blood samples were obtained from the angular vein to measure levels of stress markers, serum superoxide dismutase and malondialdehyde, using the ELISA. The expression of TRX in STZ-induced rat vascular tissue was analyzed by immunohistochemistry, quantitative polymerase chain reaction (qPCR) and western blot analysis. The oral administration of nicorandil induced TRX protein and mRNA expression in the vascular tissue of STZ-induced diabetic rats. In the diabetic control group, the levels of stress were markedly higher than those in the nicorandil-treated group, indicating that nicorandil reduces oxidative stress in serum. In addition to inducing TRX expression, nicorandil attenuated the expression of the vascular cell adhesion molecule-1 (VCAM-1) in diabetic rat vascular endothelial cells. In conclusion, nicorandil attenuates the formation of reactive oxygen species and induces TRX protein expression, consequently resulting in the suppression of VCAM-1 secretion in the vascular endothelial cells of STZ-induced diabetic rats.
 ...
PMID:Nicorandil attenuates endothelial VCAM-1 expression via thioredoxin production in diabetic rats induced by streptozotocin. 2467 84