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RATIONALE Endothelial progenitor cells (EPCs) contribute to the regeneration of endothelium. Aging-associated senescence results in reduced number and function of EPCs, potentially contributing to increased cardiac risk, reduced angiogenic capacity, and impaired cardiac repair effectiveness. The mechanisms underlying EPC senescence are unknown. Increasing(More)
OBJECTIVE The goal of this study was to investigate the potential role of sex hormones in coronary atherosclerosis in both men and postmenopausal women. DESIGN A total of 258 male and 236 female postmenopausal participants with angiographically defined stable coronary artery disease (CAD) were enrolled. We measured the levels of estradiol (E2),(More)
Macrophage migration inhibitory factor (MIF) involves the pathogenesis of atherosclerosis (AS) and increased plasma MIF levels in diabetes mellitus (DM) patients are associated with AS. Here, we have been suggested that MIF could be a critical contributor for the pathological process of diabetes-associated AS by using adenovirus-mediated RNA interference.(More)
Caiyu Zeng1,2, Falin Yang3*, Hong He1,2, Keqing Hu4, Xin Wang1,2, Qin Hu1,2, and Jifu Li1,2 Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan 250012, China Department of Cardiology, Qilu Hospital, Shandong University, Jinan 250012, China(More)
Endothelial progenitor cells (EPCs) are associated with vascular repairing and progression of atherosclerotic lesion. It may lead to coronary artery disease (CAD) if circulating EPCs lose their function. Continuous nitroglycerin (NTG) therapy causes increased vascular oxidative stress and endothelial dysfunction. The aim of this study was to investigate the(More)
ICI182,780 is used in adjuvant therapies of breast cancer. As a complete estrogen receptor (ER) blocker, ICI182,780 may antagonize the effects of estrogen on the cardiovascular system. Estrogen inhibits the proliferation of vascular smooth muscle cells (VSMCs), which is one of the mechanisms that estrogen can exert cardioprotective effects. In the present(More)
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