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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

BPC 157 and Blood Vessels

Author(s): Sven Seiwerth, Luka Brcic, Lovorka Batelja Vuletic, Danijela Kolenc, Gorana Aralica, Marija Misic, Anita Zenko, Domagoj Drmic, Rudolf Rucman and Predrag Sikiric

Volume 20, Issue 7, 2014

Page: [1121 - 1125] Pages: 5

DOI: 10.2174/13816128113199990421

Price: $65

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Abstract

This review focuses on the described effects of BPC 157 on blood vessels after different types of damage, and elucidate by investigating different aspects of vascular response to injury (endothelium damage, clotting, thrombosis, vasoconstriction, vasodilatation, vasculoneogenesis and edema formation) especially in connection to the healing processes. In this respect, BPC 157 was concluded to be the most potent angiomodulatory agent, acting through different vasoactive pathways and systems (e.g. NO, VEGF, FAK) and leading to optimization of the vascular response followed, as it has to be expected, by optimization of the healing process.

Formation of new blood vessels involves two main, partly overlapping mechanisms, angiogenesis and vasculogenesis. The additional mechanism of arteriogenesis is involved in the formation of collaterals. In conjunction with blood vessel function, we at least have to consider leakage of fluid/proteins/plasma, resulting in edema/exudate formation as well as thrombogenesis. Blood vessels are also strongly involved in tumor biology. In this aspect, we have neoangiogenesis resulting in pathological vascularization, vascular invasion resulting in release of metastatic cells and the phenomenon of homing resulting in formation of secondary tumors – metastases.

Keywords: Vasculogenesis, embryonic/fetal, primary development; Angiogenesis, healing tumors, adults; Arteriogenesis, hypoxia/occlusion induced, secondary, adults; Blood vessel leakage, pressure induced, minimal vessel wall damage induced, edema; Blood vessel leakage, vessel wall damage induced, exudate; Blood vessel obstruction, vessel wall damage, thrombosis.


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