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Thioredoxin in coronary culprit lesions: possible relationship to oxidative stress and intraplaque hemorrhage
Kensaku Nishihira1, Atsushi Yamashita, Takuroh Imamura
1Division of Circulatory and Body Fluid Regulation, Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Insights
Thioredoxin (TRX), an antioxidant protein, is elevated in unstable angina pectoris (UAP) patients, correlating with plaque instability markers like hemorrhage and thrombus formation. This suggests TRX may indicate vulnerable coronary lesions.
Area of Science:
- Cardiovascular Biology
- Oxidative Stress Research
- Atherosclerosis Pathogenesis
Background:
- Thioredoxin (TRX) is a key antioxidant protein.
- Atherosclerotic plaque instability is a major cause of acute coronary syndromes.
- Oxidative stress plays a critical role in atherosclerosis.
Purpose of the Study:
- To investigate thioredoxin (TRX) expression in stable (SAP) versus unstable angina pectoris (UAP) patients.
- To determine the relationship between TRX and markers of plaque instability in coronary atherectomy specimens.
- To explore the association of TRX with oxidized low-density lipoprotein (ox-LDL), hemorrhage, and iron deposition.
Main Methods:
- Histological assessment of atherectomy specimens from SAP and UAP patients.
- Immunohistochemical analysis for macrophage, TRX, oxidized low-density lipoprotein (ox-LDL), and glycophorin A (intraplaque hemorrhage).
- Assessment of transition metal iron (Fe(2+), Fe(3+)) deposition.
Main Results:
- TRX, macrophage, and ox-LDL expression were significantly higher in UAP patients compared to SAP patients.
- Intraplaque hemorrhage and iron deposition were more pronounced in UAP lesions.
- TRX and ox-LDL positively correlated with iron deposition and thrombus formation.
Conclusions:
- TRX is upregulated in unstable coronary artery lesions, likely due to increased oxidative stress.
- TRX expression is associated with intraplaque hemorrhage and thrombus formation.
- TRX may serve as a valuable biomarker for coronary plaque instability.
Abstract:
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.
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