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Vesugen Bioregulator Peptide: Enhancing Blood Flow & Repairing Leaky Blood Vessels



Let's dive into the bioregulator peptide vesugen and its profound effects on circulation, blood vessels, hypoxia, and even aspects like athletic performance. My initial intrigue in vesugen stems from the circulatory complications tied to my Lyme and mold-induced Chronic Inflammatory Response Syndrome (CIRS). In CIRS, the endothelial blood vessel wall often sustains significant damage due to factors like high MMP-9 levels or even the hemolysins released by MARCoNs. Additionally, the rampant inflammatory cytokines in CIRS can constrict capillaries, leading to hypoxia.


Now, to frame our discussion, let's trace back to the origins of blood cell formation. Hematopoiesis in the bone marrow gives rise to all blood cells. This process hinges on the versatility of hematopoietic stem cells (HSCs), which can both self-renew and differentiate into specialized cells. Their decisions on proliferation and differentiation are influenced by a myriad of factors, from the bone marrow's immediate microenvironment to broader systemic hormonal factors. An imbalance in the body can disrupt this intricate system, impacting almost every physiological function.


Delving deeper, progenitor cells are the bridge between multipotent HSCs and fully differentiated blood cells. Myeloid progenitors can evolve into a range of cells, from red blood cells to granulocytes to platelets to monocytes, while lymphoid progenitors lead to lymphocytes. For simplicity, we'll follow the differentiation path from myeloid progenitor to erythrocytes. Erythropoietin (EPO) produced by the kidney predominantly governs this transformation, stimulating red blood cell production in response to low oxygen levels.


As erythrocytes mature, they undergo significant changes, discarding their nucleus and organelles, and adopting a biconcave shape, essential for efficient gas exchange. Once matured, they navigate into blood vessels (within the bone marrow) known as sinusoids. Here, they pass through specialized endothelial cell gaps, entering the bloodstream to perform vital roles.


The Importance of Endothelial Cells in the Vascular Wall


With this foundational knowledge, let's scrutinize the vascular wall's anatomy. It comprises three layers: the innermost tunica intima (endothelial cells), the middle elastic tunica media (smooth muscle cells), and the outer, supportive tunica externa (collagen and fibroblasts). A pivotal component of the tunica intima is the endothelial cells, which dictate vascular permeability, control blood flow / produce nitric oxide (which stimulates the smooth muscle cells to allow for blood vessel dilation), manage inflammation, and even contribute to angiogenesis. Their malfunction can create complications like edema and hypoxia to just name a couple.


Vesugen Bioregulator Peptide


Now, onto vesugen. This bioregulator peptide, with its unique tripeptide structure, has the remarkable ability to augment the proliferation of endothelial cells by influencing the DNA's protein synthesis processes. This restoration capability proves invaluable in scenarios like vascular injury or diseases like diabetes that compromise endothelial function. Beyond that, vesugen's impact on the blood-brain barrier points to its potential in combatting neuroinflammation and related diseases (including Alzheimer's Disease - check out the research article below for more info on this).


In a nutshell, vesugen holds promise in enhancing vascular function, promoting nitric oxide production vital for athletic prowess, and bolstering the overall circulatory system.


Research:


Khavinson VKh, Tarnovskaia SI, Lin'kova NS, Guton EO, Elashkina EV. [Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging]. Adv Gerontol. 2014;27(1):108-14. Russian. PMID: 25051766.


Kraskovskaya, N.A., Kukanova, E.O., Lin’kova, N.S. et al. Tripeptides Restore the Number of Neuronal Spines under Conditions of In Vitro Modeled Alzheimer’s Disease. Bull Exp Biol Med 163, 550–553 (2017). https://doi.org/10.1007/s10517-017-3847-2


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