4 results match your criteria: "Beijing Chaoyang Hospital-Affiliate of Beijing Capital Medical University[Affiliation]"
Aging aggravates nitrate-mediated ROS/RNS changes.
Oxid Med Cell Longev
December 2014
Department of Cardiology, Beijing An Zhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing 100029, China.
Nitrates are the most frequently prescribed and utilized drugs worldwide. The elderly are a major population receiving nitrate therapy. Both nitrates and aging can increase in vivo reactive oxygen species (ROS) and reactive nitrogen species (RNS).
View Article and Find Full Text PDFInhibition of Fas-associated death domain-containing protein (FADD) protects against myocardial ischemia/reperfusion injury in a heart failure mouse model.
PLoS One
June 2014
Center for Translational Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania, United States of America ; Department of Gerontology, Beijing Chaoyang Hospital-Affiliate of Beijing Capital Medical University, Beijing, China.
Aim: As technological interventions treating acute myocardial infarction (MI) improve, post-ischemic heart failure increasingly threatens patient health. The aim of the current study was to test whether FADD could be a potential target of gene therapy in the treatment of heart failure.
Methods: Cardiomyocyte-specific FADD knockout mice along with non-transgenic littermates (NLC) were subjected to 30 minutes myocardial ischemia followed by 7 days of reperfusion or 6 weeks of permanent myocardial ischemia via the ligation of left main descending coronary artery.
Aging might augment reactive oxygen species (ROS) formation and affect reactive nitrogen species (RNS) level after myocardial ischemia/reperfusion in both humans and rats.
Age (Dordr)
August 2013
Department of Gerontology, Beijing Chaoyang Hospital-Affiliate of Beijing Capital Medical University, 8 Gongtinan Road, Beijing, 100020, People's Republic of China.
Previous studies indicate aging results in significantly decreased cardiac function and increased myocardial apoptosis after myocardial ischemia/reperfusion (MI/R) in humans or rats. The underlying mechanisms of aging-exacerbated effects remain unknown. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are known to play vital roles in aging-related MI/R injury.
View Article and Find Full Text PDFPostconditioning attenuates myocardial injury by reducing nitro-oxidative stress in vivo in rats and in humans.
Clin Sci (Lond)
March 2011
Beijing Chaoyang Hospital-Affiliate of Beijing Capital Medical University, Beijing, People's Republic of China.
Article Synopsis
- The study investigates how postconditioning (postcon) protects the heart from damage after an acute myocardial infarction (AMI) by lowering levels of peroxynitrite (ONOO-) and reducing oxidative stress caused by inducible nitric oxide synthase (iNOS).
- In clinical trials on AMI patients, postcon was shown to decrease iNOS activity and plasma nitrotyrosine levels, leading to improved heart function compared to control subjects.
- Animal experiments confirmed these findings, showing that postcon lowered both iNOS activity and myocardial infarct size, while using an iNOS inhibitor mimicked postcon's effects, and an ONOO- donor negated its benefits, indicating that the cardioprotective mechanism involves