Vesugen (KED): Research Overview
Khavinson bioregulator tripeptide studied in blood vessel and vascular ageing research.
Also known as KED · Lys-Glu-Asp
What is Vesugen?
Vesugen is a Khavinson bioregulator tripeptide developed at Russia's St. Petersburg Institute of Bioregulation and Gerontology. Composed of three amino acids (lysine, glutamic acid, aspartic acid), it targets the vascular system and protects blood vessels from age-related decline. Research shows it limits atherosclerosis development, decreases endothelial dysfunction, and activates stem cells.
What is Vesugen researched for?
- Protects blood vessels from age-related deterioration through gene expression regulation.
- Limits development of atherosclerotic plaques in blood vessels.
- Decreases endothelial dysfunction that contributes to cardiovascular disease.
- Regulates sirtuin 1 levels, mimicking some benefits of calorie restriction.
- Enhances mesenchymal stem cell proliferation and reduces senescence.
- Reverses senescence-associated secretory phenotype in aging cells.
How does Vesugen work?
Vesugen works through epigenetic regulation by interacting with DNA promoter regions, particularly affecting Ki-67 gene expression which controls cell division. It plays a prominent role in regulating sirtuin 1 (SIRT1) protein levels - a key anti-aging protein activated during calorie restriction.
References
Khavinson Peptide Bioregulators Research
Advances in Gerontology · 2020
Comprehensive review of bioregulator peptides including Vesugen and their epigenetic mechanisms.
Review or meta-analysis
Short Peptides and Vascular Aging
Bulletin of Experimental Biology and Medicine · 2018
Short peptides regulate sirtuin 1 levels and protect vascular tissue from aging.
Mesenchymal Stem Cell Activation by Peptide Bioregulators Cell Technologies in Biology and Medicine
2019
Vesugen enhances MSC proliferation and reduces senescence markers in stem cells.
Common questions
Does Vesugen reduce senescent cell burden or just prevent new senescence?
Vesugen reduces senescence markers and reverses the Senescence-Associated Secretory Phenotype (SASP) in aging cells through stem cell activation and epigenetic regulation. This suggests it may reduce existing senescent cells, though the primary mechanism is prevention and restoration rather than elimination of aged cells.