免疫细胞亚群平衡在动脉粥样硬化中的机制与中医药调节作用的研究进展

动脉粥样硬化(As)是由调控促炎与抗炎平衡的免疫细胞及细胞因子等共同参与的慢性炎症性疾病,适应性免疫细胞在其中发挥重要作用.中医药因多途径、多靶点的优势疗效广泛应用于防治As.本文就As炎症反应中适应性免疫系统不同细胞亚群协同发挥促炎、抗炎的作用机制及中医药调节免疫平衡对As的影响作一综述.     

低氧诱导因子在心血管疾病中的研究进展

低氧诱导因子(HIF)为缺氧敏感性转录因子,是细胞对缺氧反应的主要调节因子,可诱导炎症、脂质代谢、内皮功能障碍、血管平滑肌细胞(VSMC)增殖,调控心血管疾病(CVD)的发生发展。该文综述了近年来HIF在CVD中的作用及作用机制的研究进展,讨论HIF对血管构成细胞类型的作用及机制以及与CVD发生发展之间的关系,可为解析CVD的发病机制和发现新的治疗靶点提供参考,旨在为进一步了解HIF在CVD发病机制中的作用及机制提供理论参考,并为设计靶向HIF的新型有效治疗药物提供依据。     

白细胞介素37与动脉粥样硬化关系的研究进展

动脉粥样硬化(As)作为一种血管的慢性炎症性疾病,是冠心病、脑梗死、外周血管疾病的主要原因,严重威胁着人类的健康和生命。白细胞介素37是白细胞介素1家族的新型抗炎分子,在炎症性疾病、肿瘤、自身免疫性疾病中发挥抗炎及免疫抑制作用,该作用的发挥可能与白细胞介素18结合蛋白、Smad3相关。目前临床及动物试验均证实白细胞介素37参与了As的病理生理过程,可通过抑制巨噬细胞、肥大细胞、树突状细胞的功能,促进Treg细胞的分化而起到抗As的作用。本文拟对白细胞介素37与As关系的研究进展作一综述。     

ncRNA调控细胞程序性死亡影响动脉粥样硬化的研究进展

动脉粥样硬化(As)是许多心血管疾病(CVD)的发病基础,巨噬细胞、平滑肌细胞和内皮细胞是参与As病变的主要细胞,诸多研究证实上述细胞程序性死亡(PCD)可影响As的发生发展,调控上述PCD可能成为防治As的关键。近年来许多研究发现非编码RNA(ncRNA)通过调控相关因子参与PCD,如凋亡、自噬、焦亡、坏死性凋亡、铁死亡和铜死亡等。该文对ncRNA通过调控PCD影响As的机制展开讨论,为As的治疗提供新思路。     

三氧化二砷洗脱支架抑制猪损伤冠状动脉局部炎性因子的表达

目的 探讨三氧化二砷(As2O3)多聚左旋乳糖酸(PLLA)涂层支架对猪损伤冠状动脉局部炎性因子表达及炎性细胞浸润的影响,了解As2O3洗脱支架对局部炎性反应的作用. 方法 在8只小型家猪的前降支、回旋支和右冠状动脉随机双盲植入裸金属支架(裸支架组)、西罗莫司洗脱支架和As2O3洗脱支架,7 d处死,检测支架段血管单核细胞趋化蛋白(MCP)-1、白细胞介素(IL)-6蛋白和mRNA表达,HE和免疫组化检测炎性细胞浸润,体外观察As2O3对人T淋巴细胞的凋亡诱导作用. 结果裸支架组MCP-1蛋白和mRNA表达分别为0.857±0.053和0.724±0.027,IL-6蛋白和mRNA表达分别为0.551±0.032和1.015±0.041,As2O3洗脱支架和西罗莫司洗脱支架均降低支架段血管MCP-1(分别为0.421±0.055和0.406±0.042)和IL-6(分别为0.151±0.032和0.146±0.051)蛋白的表达(P＜0.01),并同时降低MCP-1(分别为0.338±0.047和0.327±0.051)和IL-6(分别为0.531±0.052和0.523±0.061)mRNA的表达(P＜0.01),As2O3洗脱支架和西罗莫司洗脱支架段血管局部炎性细胞浸润较裸支架组明显减少.体外细胞培养显示,As2O3具有诱导入T淋巴细胞凋亡作用. 结论 As2O3洗脱支架具有减少猪损伤冠状动脉炎性细胞浸润和抑制炎性因子MCP-1、IL-6表达的作用,诱导炎性细胞凋亡可能是其抗炎机制之一.     

细胞焦亡在心血管疾病中作用的研究进展

心血管疾病(CVD)已成为全球范围内的主要死亡原因之一。尽管目前对CVD的研究已取得一定进展,但仍有诸多问题有待进一步研究。近年新发现的细胞焦亡是一种伴随着炎症反应的细胞程序性死亡,研究显示其在CVD的发生发展中发挥重要作用。本文对细胞焦亡在动脉粥样硬化、心肌梗死、糖尿病性心肌病、心肌炎等CVD中的作用及机制进行了综述。     

调节性T细胞在动脉粥样硬化发生机制中作用的研究进展

动脉粥样硬化(As)是动脉血管壁的一种慢性炎症性病变,相关免疫机制参与其发生、发展过程。调节性T细胞(Treg)是一种具有独特免疫调节功能的T淋巴细胞亚群,大量证据表明,Treg的数量变化和功能障碍与As的发病机制密切相关。文章简要阐述Treg在As发展中的作用机制,并介绍了Treg作为一种新型药物治疗靶点在预防和治疗As中的最新研究进展,以期对动脉粥样硬化性疾病的发生与防治提供新思路。     

炎性反应、阻塞性睡眠呼吸暂停综合征、动脉粥样硬化三者关系的研究进展

阻塞性睡眠呼吸暂停综合征(OSAS)是一种临床常见疾病,大量研究表明OSAS与心血管疾病(CVD)密切相关。动脉粥样硬化是CVD的主要病理改变,也是联系OSAS与CVD的关键。近年研究证实,炎性反应在动脉粥样硬化的发生和发展过程中具有重要作用,且CVD是炎性反应导致动脉粥样硬化所引发的最终事件。本文主要讨论了炎性反应、OSAS、动脉粥样硬化三者间的关系。     

阿克曼氏菌与动脉粥样硬化关系的研究进展

动脉粥样硬化(As)是一种复杂的慢性炎症性疾病,是导致缺血性心脏病和中风在内的心血管疾病(CVD)的主要病因,在世界范围内造成很高的发病率和死亡率。近年来,肠道菌群在As中的作用受到广泛关注。而阿克曼氏菌作为一种重要的抗As作用的有益菌却少有综述。深入探讨As发病机制及潜在治疗方法是当前医学发展的焦点。因此,文章就阿克曼氏菌如何发挥抗As作用及与抗As药物之间的关系予以综述。     

环状RNA在动脉粥样硬化中的研究进展

环状RNA(circRNA)是一类新型内源性非编码RNA,广泛存在于真核生物体中,因其含量丰富、序列保守、结构稳定等特性,是近年来热门的基因表达调节因子。越来越多的研究表明circRNA在影响内皮完整性、血管平滑肌细胞和免疫炎症细胞的功能,以及在驱动动脉粥样硬化(As)斑块起始和稳定中发挥重要作用,因此其可能作为As新型诊断生物标志物和治疗靶标。因此,文章就circRNA在As中研究现状,综述其在As中的功能以及调节机制。     

Systemic lupus erythematosus and cardiovascular disease

Atherosclerosis is an inflammatory disease characterised by presence of activated immune competent cells in middle-sized and large arteries and is the major cause of cardiovascular disease (CVD). The risk of CVD is very high in systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are, therefore, important clinical problems but may in addition also have implications for the role of immune reactions in CVD in general. Others and we have recently demonstrated that risk factors for CVD in SLE are both traditional and non-traditional acting in concert. Traditional risk factors implicated in SLE include, for example, dyslipidemia (especially high triglycerides), hypertension, renal disease, non-traditional as inflammation, antiphospholipid antibodies (aPL) and low-density lipoprotein (LDL) oxidation are also associated with CVD in SLE. Atherothrombosis is likely to be a major underlying mechanism and is not only an increased risk of thrombosis per se. It is possible that factors like proinflammatory reactions or prothrombotic factors, such as aPL, make atherosclerotic lesions in SLE more prone to rupture than in 'normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients is presently not clear. Treatment of patients with SLE should include a close monitoring of traditional risk factors and also the above-mentioned non-traditional for CVD.     

SLE, atherosclerosis and cardiovascular disease

Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE-related atherosclerosis when compared with 'normal' atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in 'normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE-related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions.     

Pathogenic immunity in systemic lupus erythematosus and atherosclerosis: common mechanisms and possible targets for intervention

Systemic lupus erythematosus (SLE) is an autoimmune disorder that primarily affects young women and is characterized by inflammation in several organs including kidneys, skin, joints, blood and nervous system. Abnormal immune cellular and humoral responses play important roles in the development of the disease process. Impaired clearance of apoptotic material is a key factor contributing to the activation of self‐reactive immune cells. The incidence of atherosclerotic cardiovascular disease (CVD) is increased up to 50‐fold in patients with SLE compared to age‐ and gender‐matched controls, and this can only partly be explained by traditional risk factors for CVD. Currently, there is no effective treatment to prevent CVD complications in SLE. Traditional preventive CVD therapies have not been found to significantly lower the incidence of CVD in SLE; therefore, there is a need for novel treatment strategies and increased understanding of the mechanisms involved in the pathogenesis of CVD complications in SLE. The pathogenic immune responses in SLE and development of atherosclerotic plaques share some characteristics, such as impaired efferocytosis and skewed T‐cell activation, suggesting the possibility of identifying novel targets for intervention. As novel immune‐based therapies for CVD are being developed, it is possible that some of these may be effective for the prevention of CVD and for immunomodulation in SLE. However, further understanding of the mechanisms leading to an increased prevalence of cardiovascular events in SLE is critical for the development of such therapies.     

Mast cells in rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic disease of joints that is characterized by inflammation, abnormal cellular and humoral immune responses, and synovial hyperplasia. Mast cells (MCs) are involved in several of these inflammatory and immune events. MC-derived mediators induce edema, destroy connective tissue, and are involved in lymphocyte chemotaxis and infiltration and in pathological fibrosis of RA joints. Moreover, MCs are involved in angiogenesis during RA, and their proteolytic activity results in cartilage destruction and bone remodeling. Lastly, MCs could be a target in the treatment of RA.     

Cellular immune dysfunction in immune thrombocytopenia (ITP)

Over the past decades, a wealth of information has been reported about the pathogenic features of immune thrombocytopenia (ITP). To this day, however, it is unclear whether the immune abnormalities associated with ITP play causative roles in the disease or are secondary epiphenomena brought on by the inflammatory processes that are associated with the disorder. Like the majority of all autoimmune diseases, ITP is an organ‐specific disease and abnormalities in immune cell types, such as antigen‐presenting cells (APC), T cells and B cells have been shown to play some sort of role in the initiation and/or perpetuation of the disease. This review will discuss recent advances in understanding three immune cells important in ITP pathophysiology: APC, T cells and B cells, and will review how they interact with each other to initiate and perpetuate ITP, particularly the chronic form of the disorder. It will also focus on new data related to the genetics of the disorder and discuss relevant animal models of ITP.     

树突状细胞与慢性阻塞性肺疾病

慢性阻塞性肺疾病（COPD）是一种慢性炎症性疾病,其病灶局部存在中性粒细胞、巨噬细胞和T淋巴细胞（尤其是CD8^＋T细胞）浸润。吸烟是COPD发病的首要诱因,目前已证实T细胞对于吸烟所致COPD的发生发展具有重要作用;树突状细胞（DCs）是已知的功能最强的抗原提呈细胞,可激活初始T细胞,在诱导和调节免疫应答中发挥关键作用。近年来发现DCs也存在于COPD病灶中,且其功能和数量均发生了改变,提示其可能与吸烟所致COPD的发病机制有关。     

免疫细胞在动脉粥样硬化炎症进展中的双刃剑作用

炎症在动脉粥样硬化发展过程中起到十分重要的作用.动脉粥样硬化病理过程由动脉内皮损伤和血浆胆固醇水平异常引起,随后通过炎症反应招募各种免疫细胞进入动脉内膜参与斑块的形成与进展,这些细胞包括巨噬细胞、树突状细胞、平滑肌细胞、T细胞、B细胞和肥大细胞等.其中每一种免疫细胞又由促炎亚群和抗炎亚群共同组成,并产生相应的促炎因子与...     

肠道菌群与动脉粥样硬化的关系

动脉粥样硬化(As)是心血管疾病(CVD)的主要病理基础且其发病机制具有多样性。肠道菌群失调可通过代谢和免疫系统导致代谢失调和炎症反应,导致斑块形成和破裂,细菌感染在As形成和斑块的发展也具有一定的影响。同时肠道菌群失调可改变胆固醇代谢和菌群代谢物如氧化三甲胺(TMAO)、胆汁酸(BAs)和短链脂肪酸(SCFAs)水平影响As发病进程。目前以肠道菌群为靶点治疗As的研究逐渐深入,益生菌、益生元、粪菌移植、中药可能是未来As治疗的潜在方法并使CVD患者获益。