TY - JOUR
T1 - Restenosis
T2 - Emerging molecular targets: Going beyond drug-eluting stents
AU - Chen, Xiaoguang
AU - Fujise, Ken
N1 - Funding Information:
Dr. Ken Fujise is an Established Investigator of the American Heart Association (0540054N). The current study was supported in part by grants from the National Institutes of Health (HL04015 and HL68024) (to K.F.) and the Roderick Duncan MacDonald General Research Fund at St. Luke's Episcopal Hospital (04RDM013) (to K.F.).
PY - 2005
Y1 - 2005
N2 - Within a few decades atherosclerosis and coronary artery diseases will be a global disease. Percutaneous coronary intervention (PCI), one of the most important treatment strategies for CAD, will thus be utilized much more extensively. Restenosis will remain the most common and feared complication of PCI, even with the widespread use of drug-eluting stents (DES). Two distinct processes contribute to restenosis: The increased cellular mass in the intima (neointimal proliferation) and the negative remodeling of the artery. A new molecular approach will lead to the discovery of effective antirestenosis molecules that block both neointimal proliferation and negative remodeling. Vascular smooth muscle cells will be the most promising cell type to be targeted.
AB - Within a few decades atherosclerosis and coronary artery diseases will be a global disease. Percutaneous coronary intervention (PCI), one of the most important treatment strategies for CAD, will thus be utilized much more extensively. Restenosis will remain the most common and feared complication of PCI, even with the widespread use of drug-eluting stents (DES). Two distinct processes contribute to restenosis: The increased cellular mass in the intima (neointimal proliferation) and the negative remodeling of the artery. A new molecular approach will lead to the discovery of effective antirestenosis molecules that block both neointimal proliferation and negative remodeling. Vascular smooth muscle cells will be the most promising cell type to be targeted.
UR - http://www.scopus.com/inward/record.url?scp=33645084784&partnerID=8YFLogxK
U2 - 10.1016/j.ddmec.2005.05.025
DO - 10.1016/j.ddmec.2005.05.025
M3 - Review article
AN - SCOPUS:33645084784
SN - 1740-6765
VL - 2
SP - 1
EP - 9
JO - Drug Discovery Today: Disease Mechanisms
JF - Drug Discovery Today: Disease Mechanisms
IS - 1
ER -