Adventitial Contributions of the ERK and Akt Pathways to Neointimal Hyperplasia
暂无分享,去创建一个
[1] M. Kibbe,et al. Effect of nitric oxide on neointimal hyperplasia based on sex and hormone status. , 2011, Free radical biology & medicine.
[2] D. Mozaffarian,et al. Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. , 2009, Circulation.
[3] Nick D. Tsihlis,et al. The role of nitric oxide in the pathophysiology of intimal hyperplasia. , 2007, Journal of vascular surgery.
[4] E. Edelman,et al. Vascular Neointimal Formation and Signaling Pathway Activation in Response to Stent Injury in Insulin-Resistant and Diabetic Animals , 2005, Circulation research.
[5] S. Epstein,et al. Akt Controls Vascular Smooth Muscle Cell Proliferation In Vitro and In Vivo by Delaying G1/S Exit , 2003, Circulation research.
[6] E. Jones,et al. Twenty-Year Survival After Coronary Artery Surgery: An Institutional Perspective From Emory University , 2003, Circulation.
[7] Reynold A Panettieri,et al. PI3K is required for proliferation and migration of human pulmonary vascular smooth muscle cells. , 2002, American journal of physiology. Lung cellular and molecular physiology.
[8] J. Vinten-johansen,et al. Perivascular Responses after Angioplasty Which May Contribute to Postangioplasty Restenosis , 2001, Annals of the New York Academy of Sciences.
[9] J. Bonnet,et al. Kinetics of adventitial repair in the rat carotid model , 2001, Coronary artery disease.
[10] M. Mann,et al. Cell Cycle Protein Expression in Vascular Smooth Muscle Cells In Vitro and In Vivo Is Regulated Through Phosphatidylinositol 3-Kinase and Mammalian Target of Rapamycin , 2001, Arteriosclerosis, thrombosis, and vascular biology.
[11] R. Nemenoff,et al. Hypoxia-induced Proliferative Response of Vascular Adventitial Fibroblasts Is Dependent on G Protein-mediated Activation of Mitogen-activated Protein Kinases* , 2001, The Journal of Biological Chemistry.
[12] A. Zalewski,et al. Adventitial myofibroblasts contribute to neointimal formation in injured porcine coronary arteries. , 1996, Circulation.
[13] M. Reidy,et al. Mechanisms of stenosis after arterial injury. , 1983, Laboratory investigation; a journal of technical methods and pathology.