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Titlebook: Atherogenesis and Aging; Sandra R. Bates,Edwin C. Gangloff Book 1987 Springler-Verlag New York Inc. 1987 cardiovascular.endothelium.metabo

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发表于 2025-3-21 19:07:56 | 显示全部楼层 |阅读模式
期刊全称Atherogenesis and Aging
影响因子2023Sandra R. Bates,Edwin C. Gangloff
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图书封面Titlebook: Atherogenesis and Aging;  Sandra R. Bates,Edwin C. Gangloff Book 1987 Springler-Verlag New York Inc. 1987 cardiovascular.endothelium.metabo
影响因子Age is a nonreversible risk factor for atherosclerosis. The atherosclerotic process begins early in life, progresses during the middle years, and usually culminates in clinical disease towards the later years of the life span. Since atherosclerosis is a multifactorial disease, and many of the "risk factors" are time- and age­ related, it has been difficult to sort out intrinsic aging from environmental factors that operate over many years. Furthermore, the role of genetic factors remains unknown. This workshop has produced much worthwhile information that is helping elucidate the impact of age on atherogenesis. Important strides have been made in understanding the role of changes in the arterial wall and of lipoproteins, platelets, and monocyte-derived macrophages in the disease process. In parallel, our understanding of the biology of aging has increased sufficiently so that these two areas of interest can now profitably intersect. The proceedings of this successful workshop emphasize that there is much to be gained by continued interaction between those scientists interested in the biology of aging at all levels and those interested in the atherosclerotic process. Hopefully, we m
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发表于 2025-3-21 21:05:39 | 显示全部楼层
Aging, Lipoprotein Metabolism, and Atherosclerosis: A Clinical Conundrumvable model, combines primary aging with alterations in those factors known to participate in atherogenesis: hypertension, dyslipoproteinemia, coagulation, and forces interfering with the integrity of the arterial endothelial barrier. Yet a third model combines the first two models but introduces ph
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Alterations in the Arterial Wall with Agings when exposed to the same risk factors. Studies with animal models, such as pigeons, suggest these differences could be genetically mediated (3). If one accepts the possibility that differences in susceptibility and resistance to atherosclerosis may, in part, be mediated at the level of the arteria
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Clonal Senescence of Vascular Smooth Muscle and Atherogenesisprague 1972; Martin and Sprague 1973; Martin et al1975a). I do so for three reasons. One, new research (Guyton et al 1980; Hoover et al 1980; Rosenberg et al 1984; Rosenberg 1985; Fritze et al 1985) now implicates the synthesis and release, from replicative vascular smooth muscle cells, of a specifi
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Melanie C. Steffens,Irena D. Eberts when exposed to the same risk factors. Studies with animal models, such as pigeons, suggest these differences could be genetically mediated (3). If one accepts the possibility that differences in susceptibility and resistance to atherosclerosis may, in part, be mediated at the level of the arteria
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