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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Expert Rev Cardiovasc Ther. 2019 Jan 9;17(3):177–184. doi: 10.1080/14779072.2019.1563483

Figure 1: Event sequence in the pathophysiology of neointimal hyperplasia (NIH):

Figure 1:

Therapeutic insult creates obligatory vessel injury and inflammation, which activates platelet. Recruited platelets induce thrombus formation and release PDGF-BB, which promotes fibroblast proliferation in addition to a downstream switch in vSMC to the dedifferentiated proliferating type (potentiated by bFGF release from subendothelial injury). Additionally, endothelial injury of the vessel promotes ECM remodeling with an imbalance of matrix metalloproteinases potentiating vSMC migration via exposure of elastin components.

EC endothelial cell, ECM – extracellular matrix, PDGF-BB – platelet derived growth factor-BB; bFGF- basic fibroblast growth factor