[Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis].
Kozlov. K L KL; Bolotov. I I II; Linkova. N S NS; Drobintseva. A O AO; Khavinson. V Kh VK; Dyakonov. M M MM; Kozina. L S LS
Key Findings
- KED normalizes endothelin‑1 levels that rise in atherosclerosis and restenosis
- KED restores cell communication by increasing connexin expression
- KED raises sirtuin‑1 levels, which are linked to DNA repair and anti‑aging
Practical Outcomes
- The findings hint that KED could support vascular health and possibly have anti‑aging effects, but they come from cell‑culture work only. No human dosing or safety data exist yet, so it’s not ready for a DIY protocol, though it may be worth watching for future trials.
Summary
The study shows that the tiny peptide KED (Lys‑Glu‑Asp) can help blood vessel cells behave more normally in lab dishes, lowering a harmful molecule (endothelin‑1), fixing cell‑to‑cell connections, and boosting a longevity‑related protein (sirtuin‑1).
Abstract
Peptide KED (Lys-Glu-Asp) has vasoprotective effects and is effective substance in treatment of of atherosclerosis and other cardio-vascular disorders in elderly people. One of the probable mechanisms of biological activity of this peptide is epigenetic genes regulation. These genes can coding proteins, which are markers of endothelium functional activity. The goal of investigation was to study the KED peptide effect on signal molecules expression in normal, atherosclerotic and restenotic endothelium in vitro. It was shown, that KED peptide has normalized endothelin-1 expression, which increased during atherosclerosis and restenosis. KED peptide also restorates cells interactions by connexin expression. Geroprotective effect of KED peptide is realized by increasing of sirtuin1 expression, which has took part in DNA reparation.
Study Information
pubmed
2016