Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2.

By K. Parmar, H. B. Larman, G. Dai, Yuzhi Zhang, E. T. Wang, Sripriya N Moorthy, J. Kratz, Zhiyong Lin, M. Jain, M. Gimbrone and 1 more. Journal of Clinical Investigation, 2005

712 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/74a50cb76bbdc054cdc9b88ea3c604bf19b0f681

How researchers see this paper

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In Cardiology and Cardiovascular Medicine

1. K. Alitalo
2. J. Chiu
3. Peter Carmeliet
4. Rakesh K. Jain

In Molecular Biology

1. K. Alitalo
2. Shu Chien
3. M. Schwartz
4. Gavin Thurston
5. B. McConnell
6. H. Augustin
7. J. Chiu
8. G. Koh

Citations in the corpus

• Mechanotransduction in vascular physiology and atherogenesis (2009, background): “Induction of KLF2 is itself dependent on ERK5, the activity of which is specifically stimulated by atheroprotective flo”
• Control of vascular morphogenesis and homeostasis through the angiopoietin–Tie system (2009, background): “As such, the regulation of KLF2 controls the resting phenotype of the vascular endothelium in an Ang–Tie-dependent manner, through which it also acts as an atheroprotective molecul”
• Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives (2011, methodology): “KLF-2 is downstream of the MAPK ERK5 (444), which appears to play a central role in the expression of atheroprotective genes and maintenance of atheroprotective quiescent endothelial phenotype (143–145, 346, 444, 509).”
• Liver sinusoidal endothelial cells: Physiology and role in liver diseases. (2017, background): “the endothelial up-regulation of vasodilating agents including nitric oxide (NO) [28] (Figure”
• Mammalian Krüppel-Like Factors in Health and Diseases (2010, background): “KLF2 also inhibits thrombin-mediated activation of endothelial cells by inhibiting expression of the thrombin receptor protease activated receptor 1 (329).”
• Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology (2008, background): “On the basis of this finding and its in situ expression in atherosclerosis-protected regions, KLF2 has been suggested to underpin the molecular basis of the healthy state of flow-exposed endothelial cells”
• 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.”