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Published on: June 4, 2021
Novel pro-atherogenic molecule coupling factor 6 is elevated in patients with stroke: a possible linkage to
Tomohiro Osanai1, Naoto Fujiwara, Satoko Sasaki
1Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan. osanait@cc.hirosaki-u.ac.jp
Insights
Coupling factor 6 (CF6) is elevated in stroke patients and linked to homocysteine (Hcy) levels. Vitamin treatment reduced both CF6 and Hcy, suggesting CF6
Area of Science:
- Biochemistry
- Neurology
- Cardiovascular Research
Background:
- Homocysteine (Hcy) is a known stroke predictor.
- Nuclear factor kappa B (NF-kappaB) signaling, activated by Hcy, regulates Coupling Factor 6 (CF6).
Purpose of the Study:
- To investigate if CF6 levels are elevated in stroke patients.
- To examine the impact of vitamin treatment on CF6 and Hcy levels in stroke.
Main Methods:
- A study involving 59 Japanese stroke patients, randomly assigned to vitamin treatment (folic acid and B12) or no treatment.
- Plasma CF6 and total homocysteine (tHcy) levels were measured at admission and after 2 months.
Main Results:
- CF6 levels were higher in stroke patients compared to controls.
- Plasma CF6 and tHcy levels decreased in the vitamin-treated group, showing a weak positive correlation.
- No significant changes in CF6 or tHcy were observed in the untreated group.
Conclusions:
- CF6 is elevated in stroke patients, independent of other risk factors.
- CF6 may play a role in stroke development and presents a potential therapeutic target.
- Vitamin treatment impacts CF6 levels, highlighting its potential in stroke management.
Background And Purpose:
Homocysteine (Hcy) is an independent predictor of stroke. Coupling factor 6 (CF6) is regulated by nuclear factor kappa B (NF-kappaB) signaling which is activated by Hcy. We tested the hypothesis that CF6 is elevated with Hcy in stroke. We also examined the effect of vitamin treatment on CF6 and Hcy levels.
Methods And Results:
The 59 Japanese patients with a recent history of stroke were randomly assigned to a group without vitamin treatment (Group 1, n = 29) and to a group with treatment with both folic acid and vitamin B(12) for 2 months (Group 2, n = 30). The CF6 level was elevated in the patients with stroke compared with that in controls (n = 64) at admission. In a multiple regression model, the plasma CF6 level was weakly correlated to the total Hcy (tHcy) level. In Group 1, the plasma tHcy and CF6 levels were unchanged. In Group 2, however, they were both decreased, and there was a weak positive correlation between the decreases in plasma levels of CF6 and tHcy.
Conclusion:
CF6 is elevated in patients with stroke independently of risk factors. Since Hcy and vitamin treatment affect CF6 levels in stroke, CF6 appears to be a novel molecule for the pathogenesis and treatment of stroke.
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