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Ischemia ő a paradox waiting a solution (342.1)
Author(s) -
Isenberg Jeffrey
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.342.1
Subject(s) - angiogenesis , ischemia , medicine , wound healing , vascularity , arteriogenesis , neovascularization , perfusion , blood vessel , pathology , cancer research , immunology
Ischemia ‐ A paradox waiting a solution. The loss of vascular networks and tissue perfusion is termed ischemia and is a major contributor to delayed wound healing and cardiovascular disease. In contrast to ischemia, angiogenesis is the process of new blood vessel formation from existing vessels. Angiogenesis occurs by sprouting of endothelial cells in the vessel wall, either arterial or venous vessels. Growth factors have been identified that can promote this process and are currently being targeted, albeit with limited clinical success, to enhance wound healing and mitigate cardiovascular disease. Still, it remains unclear what mechanisms are upregulated to inhibit angiogenesis in the face of injury, ischemia and cardiovascular disease. Analysis of the convergence of ischemic and angiogenic promoting factors has identified unique potential treatment opportunities. Case in point, new research has uncovered an, as of yet, unappreciated pathway mediated by the matricellular protein thrombospondin‐1 (TSP1) that is induced with injury and in cardiovascular disease and that limits angiogenic signals to promote ischemia. Blockade of TSP1 activation of its high affinity receptor CD47 increases angiogenic signaling via multiple downstream pathways, improves tissue vascularity, increases blood flow, hastens wound healing and corrects cardiovascular disease.