|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Contribution of oxidative stress to pulmonary arterial hypertension显示文摘Recent data implicate oxidative stress as a mediator of pulmonary hypertension (PH) and of the associated pathological changes to the pulmonary vasculature and right ventricle (RV). Increases in reactive oxygen species (ROS), altered redox state, and elevated oxidant stress have been demonstrated in the lungs and RV of several animal models of PH, including chronic hypoxia, monocrotaline toxicity, caveolin-1 knock-out mouse, and the transgenic Ren2 rat which overexpresses the mouse renin gene. Generation of ROS in these models is derived mostly from the activities of the nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase. As disease progresses circulating monocytes and bone marrow-derived monocytic progenitor cells are attracted to and accumulate in the pulmonary vasculature. Once established, these inflammatory cells generate ROS and secrete mitogenic and fibrogenic cytokines that induce cell proliferation and fibrosis in the vascular wall resulting in progressive vascular remodeling. Deficiencies in antioxidant enzymes also contribute to pulmonary hypertensive states. Current therapies were developed to improve endothelial function, reduce pulmonary artery pressure, and slow the progression of vascular remodeling in the pulmonary vasculature by targeting deficiencies in either NO (PDE-type 5 inhibition) or PGI 2 (prostacyclin analogs), or excessive synthesis of ET-1 (ET receptor blockers) with the intent to improve patient clinical status and survival. New therapies may slow disease progression to some extent, but long term management has not been achieved and mortality is still high. Although little is known concerning the effects of current pulmonary arterial hypertension treatments on RV structure and function, interest in this area is increasing. Development of therapeutic strategies that simultaneously target pathology in the pulmonary vasculature and RV may be beneficial in reducing mortality associated with RV failure. | Vincent G DeMarco Adam T Whaley-Connell James R Sowers Javad Habibi Kevin C Dellsperger | 2010 | World Journal of Cardiology2010，2，10： | 21 |
| 2 | Ab-sence of TGFBR1 and TGFBR2 mutations in patients with bi-cuspid aortic valve and aortic dilation 显示文摘 | ARRINGTON C B SOWER C T CHUCKWUK N | 2008 | Am J Cardiol2008，102，5： | 1 |
| 3 | Pulmonary regurgitation:determining severity by echocardiography and magnetic resonance imaging显示文摘 | Puchalski M D Askovich B Sower C T | 2008 | Congenit Heart Dis2008，3，3： | 1 |
| 4 | First principles calculation of pKa values for 5-substituted uracils 显示文摘 | JANG Y H SOWERS L C CAGIN T | 2001 | J Phys Chern A2001，105，1： | 1 |
| 5 | Effect of nitrogen incorporation on electron emission from chemical vapor deposition diamond显示文摘 | SOWERS A T LIZZUL R C | 1999 | Journal of Vacuum Science and Technology B1999，17，： | 1 |
| 6 | Laboratory characterization of measles virus infection in previously vaccinat- ed and unvaccinated individuals显示文摘 | HICKMAN C J HYDE T B SOWERS S B | 2011 | J infect dis2011，204，1： | 1 |
| 7 | Comparison of the microbial diversity at different depths of the GISP2 Greenland ice core in relationship to deposition climates显示文摘 | Miteva V Teacher C Sowers T | 2009 | Environmental Microbiology2009，11，3： | 1 |
| 8 | Type 2 diabetes mellitus:greater cardiovascular risks and greater benefits of therapy (Editorial) 显示文摘 | Fagan T C Sowers J | 1999 | Arc Intern Med1999，159，： | 1 |
| 9 | Effect of nitrogen incurrtion on electron emission from chemical vapor deposition diamond 显示文摘 | Park M Sowers A T Lizzul Rinne C | 1999 | Vac Sci Technolo B1999，17，： | 1 |
| 10 | Type 2 diabetes mellitus : greater cardiovascular risksand greater benefits of therapy显示文摘 | Fagan T C Sowers J | 1999 | Arch Intern Med1999，159，10： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员