Prolonged fluid shear stress induces a distinct set of endothelial cell genes, most specifically lung Krüppel-like factor (KLF2).

By R. Dekker, S. van Soest, R. Fontijn, Sonia Salamanca, P. D. de Groot, E. vanBavel, H. Pannekoek, A. Horrevoets. Blood, 2002

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Anti-Inflammatory Effects of Statins: Clinical Evidence and Basic Mechanisms (2005, background): “More recently, Dekker and colleagues found that KLF2 was induced by laminar shear stress and that its expression in human aorta was robust in linear segments of the arterial tree but deficient at branch points, regions that are particularly prone to atherosclerotic lesion formatio”
KLF2 Is a Novel Transcriptional Regulator of Endothelial Proinflammatory Activation (2004, background): “demonstrated using normal human aortic tissue that KLF2 expression is robust in the endothelium except at branch points where expression is nearly absent (28).”
Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology (2008, background): “antioxidative, anti-inflammatory, antiproliferative) and in situ endothelial expression of candidate genes at locations that are protected from atherosclerosis”
Mammalian Krüppel-Like Factors in Health and Diseases (2010, background): “predicted to be exposed to laminar shear stress (108).”
Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis (2016, neutral): “focused on transcriptional regulators.(161,165,166) Among the transcription factors most responsive to hemodynamic stimuli, the zinc finger transcription factor, Kruppel-like factor 2 (KLF2), seemed to show the strongest differential upregulation by atheroprotective waveform stimulation.”