亲环素A在动脉粥样硬化发展进程中研究进展

动脉粥样硬化(AS)是冠心病发生的重要病理基础,是血管慢性非特异性炎症病变.参与AS形成的多种细胞可分泌亲环素A(CyPA).作为一种炎症因子,CyPA能与相关的炎症细胞及炎症介质相互作用,促进AS斑块的发生与发展.     

NLRP3炎症小体在动脉粥样硬化相关细胞中作用的研究进展

炎症小体是一种调控IL-1β产生的大分子多蛋白复合体,在动脉粥样硬化(atherosclerosis,As)病变发生发展中发挥重要作用。NLRP3炎症小体是目前研究最为深入和广泛的炎症小体类型。该文主要通过总结AS相关细胞(内皮细胞、巨噬细胞、血管平滑肌细胞)与NLRP3炎症小体之间的关系来探讨NLRP3炎症小体在AS病变发生发展中的作用。     

血管细胞黏附分子-1与动脉粥样硬化机制的研究现状北大核心CSCD

动脉粥样硬化(AS)是一种慢性的、以脂质发育为特征的炎症过程。血管细胞黏附分子-1(VCAM-1)是一种炎症因子,表达在炎症环境下的内皮细胞膜上,介导白细胞的滚动和黏附。在AS开始初期,免疫细胞和脂质浸润血管壁形成斑块,VCAM-1在这个过程中发挥了重要的作用。本文对目前AS发生、发展过程中VCAM-1高表达的诱因及其病理机制,以及通过减少VCAM-1表达抗AS的药物进行了综述。     

PPAR与动脉粥样硬化

动脉粥样硬化(AS)的发生是一个复杂的病理过程,其发生机制尚未完全明确。近年来炎症、免疫反应在AS发生发展中的作用越来越受到人们的重视,人们已经认识到AS也是一种炎症性疾病。过氧化物酶体增殖物激活受体(PPAR)是核受体超家族的一员,活化后与抗炎、脂质代谢、糖稳态和细胞的     

不同细胞来源的外泌体在动脉粥样硬化中的研究进展

外泌体是细胞分泌的纳米级膜微粒,能在细胞与细胞之间传递信息。外泌体参与调控细胞的生理活动,在动脉粥样硬化(atherosclerosis,AS)的发生发展中发挥重要作用。作为细胞外囊泡,外泌体受到越来越多的关注,该文综述AS相关细胞(免疫细胞、血小板、血管内皮细胞、血管平滑肌细胞)来源的外泌体在AS发病过程中的作用。     

宁心痛颗粒治疗对不稳定性心绞痛合并易损斑块患者血清学指标的影响

不稳定性心绞痛(UAP)是急性冠脉综合征(ACS)的表现形式之一,是由于冠状动脉粥样斑块破裂伴有不同程度的表面血栓形成及远端血管栓塞.导致缺血性心绞痛[1]冠状动脉粥样硬化(AS)是ACS的病理生理基础,炎症贯穿于AS病变发生、发展和恶化的全过程.炎症细胞大量激活、炎症介质水平增高、粥样斑块破裂、血栓形成等因素共同参与决定了ACS的发生和发展.     

肥大细胞与动脉粥样硬化关系研究的新进展

近年来心脑血管事件的发生日益增多,其预防及治疗引起人们的广泛关注与重视.肥大细胞(MC)是一种参与炎症免疫应答反应的炎症细胞,最近的研究表明MC与冠状动脉粥样硬化(AS)的发生发展密切相关,MC可以产生多种炎症介质,包括组胺、前列腺素、胃促胰酶、类胰蛋白酶和各种化学因子及细胞因子,它们能诱导血管炎症、内皮功能失调、泡沫细胞形成、细胞外基质降解、微血管新生以及内皮、平滑肌细胞凋亡,对斑块的形成及斑块稳定性起着重要作用.     

MCP-1、VEGF与动脉粥样硬化的关系

动脉粥样硬化(arteriosclerosis AS)是慢性炎症性疾病,主要由于血管内皮损伤、继发炎症、免疫功能障碍三者相互作用形成。血管壁慢性炎症是AS的特征,动脉硬化灶中炎性细胞主要为单核/巨噬细胞。已知单核细胞趋化蛋白-1(monocyte chermtach protein-1 MCP-1)是单核/巨噬细胞特异的趋化性因子,其主要功能是趋化和激活单核/巨噬细胞至炎症部位,参与炎症反应、调节免疫,并促进动脉粥样硬化的形成;血管内皮生长因子(Endogenous vascular endothelial growth factor VEGF)是特异血管内皮细胞促有丝分裂原,在血管内皮生成细胞增殖有关的病理过程中占首要地位,最近报道它在AS中起重要作用。     

血管紧张素Ⅱ与动脉粥样硬化

血管紧张素Ⅱ (AngⅡ )是肾素 血管紧张素系统 (RAS)中主要的活性肽产物。近年来 ,大量的研究表明 ,AngⅡ参与了动脉粥样硬化 (AS)的发生、发展。利用分子生物学等技术发现人AS斑块内存在血管紧张素转换酶 (ACE)、AngⅡ及AngⅡ受体。并且 ,斑块组织内细胞成分 (巨噬细胞、平滑肌细胞、内皮细胞及成纤维细胞 )可进一步生成RAS。因此 ,深入了解RAS在AS发生过程中起到的作用及其作用途径 ,将有助于阐明AS的发病机制。下面就AngⅡ在AS中的具体作用及作用机制加以阐述。1　AngⅡ与内皮功能失调内皮功能失调是AS最早期发生的事件之一…     

动脉粥样硬化发生过程中细胞之间的相互调控

<正> 动脉粥样硬化(以下简称AS)的并发症,是人类死亡的主要原因之一。关于AS发病机理有多种假说。近10年由于单克隆抗体技术和基因调控等分子生物学技术的应用,人们更多地注意到血管内皮细胞、平滑肌细胞、单核/巨噬细胞及血小板在AS的发生、发展过程中的相互作用。在某些致病因素作用下,这些细胞通过产生生物活性物质而相互影响,决定着AS的发生和发展。     

动脉粥样硬化血管内皮分泌功能失调与平滑肌细胞增殖

血管内皮细胞和平滑肌细胞是血管壁两种主要细胞,两者在结构上和功能上有着密切的关系,动脉粥样硬化的发生源于循环因子和血管壁细胞间的相互作用,内皮细胞损伤等所导致的分泌功能失调和平滑肌细胞的异常增殖而引起的血管腔狭窄和痉挛是动脉粥样硬化等多种血管疾病发生发展的共同病理基础。本文从动脉粥样硬化病理状态下血管内皮分泌的生长因子、细胞因子、血管活性物质对平滑肌细胞增殖影响的最新研究进展做一综述。     

吸烟、硝酸甘油对动脉粥样硬化家兔血管平滑肌细胞钙浓度的影响

目的研究吸烟、硝酸甘油对动脉粥样硬化血管平滑肌细胞胞内游离钙浓度([Ca2+]i)的影响,探讨吸烟对动脉粥样硬化形成及硝酸甘油的生物效应的作用。方法复制家兔动脉粥样硬化模型,分离血管平滑肌细胞。Fluo-3/AM负载细胞,应用流式细胞仪检测血管平滑肌细胞[Ca2+]i,激光扫描共聚焦显微系统测定单个血管平滑肌细胞内Ca2+的时空变化。结果各组动物主动脉壁均见到程度不同的动脉粥样硬化斑块形成。动脉粥样硬化家兔血管平滑肌细胞[Ca2+]i明显升高(48.45±5.31,与生理盐水对照组38.09±2.57比较,P<0.01);吸烟能增加动脉粥样硬化家兔血管平滑肌细胞[Ca2+]i(56.48±2.99,与单纯动脉粥样硬化组48.45±5.31比较,P<0.01);硝酸甘油则能明显降低动脉粥样硬化家兔血管平滑肌细胞[Ca2+]i(41.91±3.16,与单纯动脉粥样硬化组48.45±5.31比较,P<0.05);吸烟能明显抑制硝酸甘油降低血管平滑肌细胞[Ca2+]i的作用(47.99±5.10,与硝酸甘油组41.91±3.16比较,P<0.05)。结论吸烟能明显增加动脉粥样硬化血管平滑肌细胞[Ca2+]i,硝酸甘油则能明显降低动脉粥样硬化血管平滑肌细胞[Ca2+]i,吸烟能抑制硝酸甘油的生物学效应。     

The role of vascular cell senescence in atherosclerosis: antisenescence as a novel therapeutic strategy for vascular aging

Vascular cells have a finite lifespan when cultured in vitro and eventually enter an irreversible growth arrest called "cellular senescence." It has been reported that many of the changes in senescent vascular cell behavior are consistent with the changes seen in age-related vascular diseases. Recently, senescent vascular cells have been demonstrated in human atherosclerotic lesions but not in non-atherosclerotic lesions. Moreover, these cells express increased levels of proinflammatory molecules and decreased levels of endothelial nitric oxide synthase, suggesting that cellular senescence in vivo contributes to the pathogenesis of human atherosclerosis. One widely discussed hypothesis of senescence is the telomere hypothesis. An increasing body of evidence has established the critical role of the telomere in vascular cell senescence. Introduction of telomere malfunction has been shown to lead to vascular dysfunction that promotes atherogenesis, whereas telomere lengthening extends cell lifespan and protects against vascular dysfunction associated with senescence. Indeed, recent studies have demonstrated that telomere attrition occurs in the blood vessels and is associated with human atherosclerosis. More recent evidence suggests that telomere-independent mechanisms are implicated in vascular cell senescence. Activation of Ras, an important signaling molecule involved in atherogenic stimuli, induces vascular cell senescence and thereby, promotes vascular inflammation in vitro and in vivo. Although a causal link between vascular aging and vascular cell senescence remains elusive, a large body of data is consistent with cellular senescence contributing to age-associated vascular disorders. This review considers the clinical relevance of vascular cell senescence in vivo and discusses the potential of antisenescence therapy for human atherosclerosis.     

氧化低密度脂蛋白与动脉粥样硬化的研究

氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)在动脉粥样硬化(atherosclerosis AS)发病过程中的作用逐渐受到人们的重视。ox-LDL通过损伤内皮细胞、参与泡沫细胞形成、调控血管平滑肌的增殖等多个方面影响动脉粥样硬化的发生和发展。抗氧化剂的应用是治疗动脉粥样硬化的一个重要手段。     

Role of interleukin-4 in atherosclerosis

Vascular endothelial cell injury or dysfunction has been implicated in the onset and progression of cardiovascular diseases including atherosclerosis. A number of previous studies have demonstrated that the pro-oxidative and pro-inflammatory pathways within vascular endothelium play an important role in the initiation and progression of atherosclerosis. Recent evidence has provided compelling evidence to indicate that interleukin-4 (IL-4) can induce pro-inflammatory environment via oxidative stress-mediated up-regulation of inflammatory mediators such as cytokine, chemokine, and adhesion molecules in vascular endothelial cells. In addition, apoptotic cell death within vascular endothelium has been hypothesized to be involved in the development of atherosclerosis. Emerging evidence has demonstrated that IL-4 can induce apoptosis of human vascular endothelial cells through the caspase-3-dependent pathway, suggesting that IL-4 can increase endothelial cell turnover by accelerated apoptosis, the event which may cause the dysfunction of the vascular endothelium. These studies will have a high probability of revealing new directions that lead to the development of clinical strategies toward the prevention and/or treatment for individuals with inflammatory vascular diseases including atherosclerosis.     

药物治疗动脉粥样硬化新途径——抗炎作用

越来越多的实验证据和临床资料表明 ,炎症反应贯穿了动脉粥样硬化发生和发展的整个过程。炎症可以激活单核细胞和刺激内皮细胞产生促炎因子 ,进而刺激血管平滑肌细胞迁移、增殖 ,炎症继续发展 ,细胞释放的水解酶、细胞因子等进一步加重损伤 ,最终形成斑块。因此 ,根据这一新的发病机制 ,通过抗炎途径治疗动脉粥样硬化已引起人们的极大关注。该文对药物通过调节C反应蛋白、CD4 0 CD4 0L、感染和NF κB抗动脉粥样硬化的研究进展作一综述     

Involvement of the ADAM 12 in thrombin-induced rat's VSMCs proliferation

Cardiovascular disease is the largest single cause of mortality and its major underlying pathology is atherosclerosis. The proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of the various vascular diseases, including atherosclerosis and hypertension. Thrombin (Thr) is involved in the abnormal proliferation of VSMCs associated with atherosclerosis and hypertension. ADAMs (A Disintegrin And Metalloproteinase) are transmembrane metalloproteinases, belonging to the adamalysins group, that are distinct from matrix metalloproteinases (MMPs) in a way as they have an extracellular disintegrin domain and cytoplasmic domain that can associate with intracellular proteins. There is limited knowledge about the presence of ADAM metalloproteinase activity in Thr-induced VSMCs proliferation. Therefore, this review examines recent findings in signaling mechanisms employed by Thr in modulating the regulation of proliferation of VSMCs with particular emphasis on involvement of ADAM 12 which has been identified as an important mediator of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of Thr in vascular biology and vascular diseases.     

Real-time nanoscale proteomic analysis of the novel multi-kinase pathway inhibitor rigosertib to measure the response to treatment of cancer

Endothelin (ET) is a powerful vasoconstrictor that affects vascular tone and blood pressure; however, recent evidence suggests that ET acts as an autocrine or paracrine factor and plays a role in the pathogenesis of atherosclerosis. In humans and in animal models, elevated plasma ET concentrations are associated with hypercholesterolaemia and atherosclerosis. ET and its receptors are located in endothelial cells, macrophages and smooth muscle cells of atherosclerotic and arteriosclerotic lesions. In vitro, endothelial cells, macrophages and smooth muscle cells synthesise ET and express ET receptors. Oxidised low density lipoprotein (LDL), growth factors, vasoactive peptides, and cytokines induce ET gene expression and protein synthesis. Conversely ET stimulates the synthesis of growth factors, inflammatory mediators, chemokines and adhesion molecules. In animal models, ET receptor antagonists decrease fatty streak progression during hypercholesterolaemia, and inhibit the formation of a fibrous neointima following arterial balloon catheter injury. It appears likely that ET indirectly promotes several phases of atherogenesis such as monocyte diapedesis into the artery wall, and the migration and proliferation of vascular smooth muscle cells. In summary, ET appears to be intricately involved in the elaboration of paracrine and autocrine factors mediating inflammation and wound healing. Pharmacological blockade of ET receptors inhibits the development of vascular lesions as a result of either hypercholesterolaemia or physical injury. Thus, it is possible that ET receptor antagonists could be used therapeutically to treat human vascular diseases such as atherosclerosis.     

细胞自噬在动脉粥样硬化发生发展中的作用

细胞自噬是生物体内清除功能异常的细胞器、错误折叠的蛋白质、被氧化的脂类等有害大分子物质的重要途径。在动脉粥样硬化中的作用具有双重性,不仅作为抵御环境变化对细胞造成损害的防御机制,又可以诱导细胞Ⅱ型程序性死亡,如何调控自噬在动脉粥样硬化的防治中至关重要。巨噬细胞、血管内皮细胞和血管平滑肌细胞的自噬参与动脉粥样硬化发生发展过程,在斑块的形成和破裂中发挥潜在作用。深入了解细胞自噬与动脉粥样硬化的关系,将有可能为动脉粥样硬化的药物防治提供新的治疗靶点。