Abstract
Opioids are potent drugs that are widely used to control wound or cancer pain. Increasing evidence suggest that opioids mediate clinically relevant effects that go beyond their classical role as analgesics. Of note, opioids appear to modulate angiogenesis - a process that is critical in wound healing and cancer progression. In this review, we focus on pro- and anti-angiogenic facets of opioids that arise from the activation of individual opioid receptors and the usage of individual concentrations or application routes. We overview the still incompletely elucidated mechanisms of these angiogenic opioid actions. Moreover, we describe plausible opioids effects, which - although not primarily studied in the context of vessel formation - may be related to the opioid-driven processes of angiogenesis. Finally we discuss the use of opioids as an innovative therapeutic avenue for the treatment of chronic wounds and cancer.
Highlights
Angiogenesis is the formation of new blood vessel out of pre-existing ones and includes endothelial cell activation, proliferation and chemotactic-driven migration
A variety of data, provided by in-vitro, animal and clinical studies indicate that opioids modulate angiogenesis
Depending on the opioid receptor type, concentration and application route, opioids act as proor anti-angiogenic factors during wound healing and tumor growth
Summary
Angiogenesis is the formation of new blood vessel out of pre-existing ones and includes endothelial cell activation, proliferation and chemotactic-driven migration. This finding leads to the suggestion that morphine activates VEGF receptors and exploits their angiogenic signaling on endothelial cells. C-Src knock-down by siRNA prevented morphine-induced VEGF receptor activation, endothelial cell proliferation and tube formation.
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