Cardiovascular disease,predominantly coronary heart disease and stroke,leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions.The dominant pathologic foundation for cardi...Cardiovascular disease,predominantly coronary heart disease and stroke,leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions.The dominant pathologic foundation for cardiovascular disease is atherosclerosis and,as to coronary heart disease,coronary atherosclerosis and resulting lumen stenosis,even total occlusions.In translational research,several animals,such as mice,rabbits and pigs,have been used as disease models of human atherosclerosis and related cardiovascular disorders.However,coronary lesions are either naturally rare or hard to be fast induced in these models,hence,coronary heart disease induction mostly relies on surgical or pharmaceutical interventions with no or limited primary coronary lesions,thus unrepresentative of human coronary heart disease progression and pathology.In this review,we describe the progress of animal models of coronary heart disease following either spontaneous or diet-accelerated coronary lesions.展开更多
Coronary atherosclerotic heart disease had been regarded as the leading killer of human being.The atherosclerotic lesion would cause blood flow blockage or lumen stenosis of coronary arteries,thus resulting in myocard...Coronary atherosclerotic heart disease had been regarded as the leading killer of human being.The atherosclerotic lesion would cause blood flow blockage or lumen stenosis of coronary arteries,thus resulting in myocardial ischemic or sudden cardiac death.Though exact causes of coronary atherosclerosis heart disease is not known,the promising Apo C-Ⅲthat played a crucial role in metabolism of triglyceride-rich lipoproteins had been supposed to be one of the key factor of pathogenesis.In this review,we discuss roles of Apo C-Ⅲin the development of CAD and its insights being a new therapeutic target.展开更多
Objective To evaluate the relationship between plasma apoA Ⅳ levels and coronary atherosclerosis and to explore its relation to other risk factors Methods Using ELISA techniques, plasma apoA Ⅳ levels were quant...Objective To evaluate the relationship between plasma apoA Ⅳ levels and coronary atherosclerosis and to explore its relation to other risk factors Methods Using ELISA techniques, plasma apoA Ⅳ levels were quantified in 181 patients who underwent coronary angiography (CAG) Patients were divided according to their coronary status into a coronary heart disease (CHD) group (stenotic lesion on CAG, n=118) and a control group (normal CAG, n=63) The severity of atherosclerosis was assessed by stenosis scoring of the different lesions Other parameters, including apoA Ⅰ, apoB, Lp(a), HDL C, LDL C, TG, and TC, were measured as well Univariate, logistic regression analyses were used to define the relationship between coronary atherosclerosis and plasma apoA Ⅳ levels Results When compared with the control group, plasma apoA Ⅳ levels were found to be lower in the CHD group There was a weak negative correlation between plasma apoA Ⅳ levels and the severity of coronary atherosclerosis ApoA Ⅳ was found to be a relatively independent risk factor for CHD We also found a positive correlation between apoA Ⅳ and triglyceride levels Conclusions ApoA Ⅳ may be important in the prediction of CHD and coronary atherosclerosis severity It may also play an important role in the metabolism of triglycerides展开更多
Lipoprotein（a） [Lp（a）] is composed of a low density lipoprotein（LDL）-like particle to which apolipoprotein（a）[apo（a）] is linked by a single disulfide bridge. Lp（a） is considered a causal risk factor for is...Lipoprotein（a） [Lp（a）] is composed of a low density lipoprotein（LDL）-like particle to which apolipoprotein（a）[apo（a）] is linked by a single disulfide bridge. Lp（a） is considered a causal risk factor for ischemic cardiovascular disease（CVD） and calcific aortic valve stenosis（CAVS）. The evidence for a causal role of Lp（a） in CVD and CAVS is based on data from large epidemiological databases, mendelian randomization studies, and genome-wide association studies. Despite the well-established role of Lp（a） as a causal risk factor for CVD and CAVS, the underlying mechanisms are not well understood. A key role in the Lp（a） functionality may be played by its oxidized phospholipids（OxPL） content. Importantly, most of circulating OxPL are associated with Lp（a）; however, the underlying mechanisms leading to this preferential sequestration of OxPL on Lp（a） over the other lipoproteins,are mostly unknown. Several studies support the hypothesis that the risk of Lp（a） is primarily driven by its OxPL content.An important role in Lp（a） functionality may be played by the lipoprotein-associated phospholipase A_2（Lp-PLA_2）,an enzyme that catalyzes the degradation of OxPL and is bound to plasma lipoproteins including Lp（a）. The present review article discusses new data on the pathophysiological role of Lp（a） and particularly focuses on the functional role of OxPL and Lp-PLA_2 associated with Lp（a）.展开更多
文摘Cardiovascular disease,predominantly coronary heart disease and stroke,leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions.The dominant pathologic foundation for cardiovascular disease is atherosclerosis and,as to coronary heart disease,coronary atherosclerosis and resulting lumen stenosis,even total occlusions.In translational research,several animals,such as mice,rabbits and pigs,have been used as disease models of human atherosclerosis and related cardiovascular disorders.However,coronary lesions are either naturally rare or hard to be fast induced in these models,hence,coronary heart disease induction mostly relies on surgical or pharmaceutical interventions with no or limited primary coronary lesions,thus unrepresentative of human coronary heart disease progression and pathology.In this review,we describe the progress of animal models of coronary heart disease following either spontaneous or diet-accelerated coronary lesions.
文摘Coronary atherosclerotic heart disease had been regarded as the leading killer of human being.The atherosclerotic lesion would cause blood flow blockage or lumen stenosis of coronary arteries,thus resulting in myocardial ischemic or sudden cardiac death.Though exact causes of coronary atherosclerosis heart disease is not known,the promising Apo C-Ⅲthat played a crucial role in metabolism of triglyceride-rich lipoproteins had been supposed to be one of the key factor of pathogenesis.In this review,we discuss roles of Apo C-Ⅲin the development of CAD and its insights being a new therapeutic target.
文摘Objective To evaluate the relationship between plasma apoA Ⅳ levels and coronary atherosclerosis and to explore its relation to other risk factors Methods Using ELISA techniques, plasma apoA Ⅳ levels were quantified in 181 patients who underwent coronary angiography (CAG) Patients were divided according to their coronary status into a coronary heart disease (CHD) group (stenotic lesion on CAG, n=118) and a control group (normal CAG, n=63) The severity of atherosclerosis was assessed by stenosis scoring of the different lesions Other parameters, including apoA Ⅰ, apoB, Lp(a), HDL C, LDL C, TG, and TC, were measured as well Univariate, logistic regression analyses were used to define the relationship between coronary atherosclerosis and plasma apoA Ⅳ levels Results When compared with the control group, plasma apoA Ⅳ levels were found to be lower in the CHD group There was a weak negative correlation between plasma apoA Ⅳ levels and the severity of coronary atherosclerosis ApoA Ⅳ was found to be a relatively independent risk factor for CHD We also found a positive correlation between apoA Ⅳ and triglyceride levels Conclusions ApoA Ⅳ may be important in the prediction of CHD and coronary atherosclerosis severity It may also play an important role in the metabolism of triglycerides
文摘Lipoprotein（a） [Lp（a）] is composed of a low density lipoprotein（LDL）-like particle to which apolipoprotein（a）[apo（a）] is linked by a single disulfide bridge. Lp（a） is considered a causal risk factor for ischemic cardiovascular disease（CVD） and calcific aortic valve stenosis（CAVS）. The evidence for a causal role of Lp（a） in CVD and CAVS is based on data from large epidemiological databases, mendelian randomization studies, and genome-wide association studies. Despite the well-established role of Lp（a） as a causal risk factor for CVD and CAVS, the underlying mechanisms are not well understood. A key role in the Lp（a） functionality may be played by its oxidized phospholipids（OxPL） content. Importantly, most of circulating OxPL are associated with Lp（a）; however, the underlying mechanisms leading to this preferential sequestration of OxPL on Lp（a） over the other lipoproteins,are mostly unknown. Several studies support the hypothesis that the risk of Lp（a） is primarily driven by its OxPL content.An important role in Lp（a） functionality may be played by the lipoprotein-associated phospholipase A_2（Lp-PLA_2）,an enzyme that catalyzes the degradation of OxPL and is bound to plasma lipoproteins including Lp（a）. The present review article discusses new data on the pathophysiological role of Lp（a） and particularly focuses on the functional role of OxPL and Lp-PLA_2 associated with Lp（a）.
