干细胞源外泌体治疗缺血性心脏病的近况

外泌体富含各类蛋白及遗传物质,其介导细胞间的信息交流及信号转导.大量研究表明各类干细胞源的外泌体可通过其内富集的各类特异性蛋白及以microRNA为首的各类遗传物质参与各类心血管疾病,并对其治疗具有深远的临床意义.对此,本文就外泌体与缺血性心脏疾病的关系展开综述,从各类干细胞源外泌体的microRNA、蛋白、离子通道及其他方面,探讨外泌体在缺血性心脏疾病中发挥的功能和作用.     

氯吡格雷对缺血性脑血管病患者阿司匹林抵抗影响的临床研究

目的观察氯吡格雷对缺血性脑血管病患者阿司匹林抵抗（AR）的影响。方法采用全血电阻法检测88例缺血性脑血管病患者ADP诱导的血小板聚集率（PAG）,将合并AR者随机分为阿司匹林加氯吡格雷治疗组（AR-A）和阿司匹林治疗组（AR-B）,阿司匹林敏感（AS）者为敏感对照组,分别于治疗1周、2周及4周后,再次测定ADP诱导的PAG,比较各组治疗前后PAG的变化。结果缺血性脑血管病患者中,出现AR 28例（32%）。治疗2周后,AR-A组ADP诱导的PAG较治疗前明显下降,AR-B组PAG较治疗前无明显改变（P〈0.01）。治疗4周后,各组PAG较2周时无统计学差异（P〉0.05）。结论缺血性脑血管病患者中,AR的发生率较高,联合氯吡格雷治疗可以改善其AR状态。     

骨髓间充质干细胞在缺血性心脏病中的作用机制及其应用

缺血性心脏病是一类严重危害人类健康的疾病.在积极开展各种药物和介入治疗的同时,细胞疗法已成为当下心血管领域的一大热点,骨髓间充质干细胞通过移植或骨髓动员至缺血心脏后能有效改善急性心肌梗死患者短期的心功能.本文就骨髓间充质干细胞疗法在缺血性心脏病中的作用机制及其应用的最新研究成果作一综述.     

自噬在缺血性心脏病发病机制中的作用

在心肌缺血再灌注过程中可以通过多种因素诱导细胞的自噬活动,心肌细胞自噬可以保护细胞,减少细胞损失,但是自噬也可导致心肌细胞死亡。     

自体骨髓单个核细胞移植治疗缺血性心脏病临床疗效观察

目的 研究经冠状动脉内移植骨髓单个核细胞治疗缺血性心力衰竭的可行性和疗效。方法 缺血性心力衰竭病人20例，抽取骨髓用密度梯度离心法分离出骨髓单个核细胞，经外周动脉穿刺插管，将自体骨髓单个核细胞注入冠脉。比较病人的临床症状，NYHY分级和治疗后由于心血管事件造成的再住院情况。结果 病人自觉症状改善，心功能提高，ECT检查显示在缺血区有血管新生。结论 自体骨髓单个核细胞移植是安全有效的。     

SDF-1-CXCR4轴与缺血性心脏病的干细胞治疗

干细胞治疗为缺血性心脏病患者提供了一种简单、经济、有效的全新治疗方法,其早期临床实验也取得了令人振奋的结果,然而更广泛的临床应用亟需更深入的基础研究的支持。SDF-1-CXCR4轴在干细胞的动员和归巢中起着关键作用,将SDF-1与干细胞治疗结合将为缺血性心脏病的细胞治疗提供一个新的途径。本文就缺血性心脏病的干细胞治疗,SDF-1-CXCR4轴在干细胞动员和心脏损伤、修复中的作用作一综述。     

Increased frequencies of apolipoprotein ε2 and ε4 alleles in patients with ischemic heart disease

It has been demonstrated that the genetic polymorphism of apolipoprotein (apo) E is associated with atherosclerosis. Thus, in this study, we have examined the apo E allele frequencies in 109 patients with ischemic heart disease (IHD) and 576 Japanese people as controls, and we have compared these frequencies between patients with IHD and controls. The frequencies of the epsilon 2 and epsilon 4 alleles were significantly higher in patients with IHD than in the controls (epsilon 2: 8.2% vs 3.7%, epsilon 4: 17.0% vs 11.7%), whereas the frequency of the epsilon 3 allele was significantly lower in patients with IHD than in the controls (74.8% vs 84.6%). The epsilon 2-carrying patients with IHD were characterized by type III (43.8%) and IV (25.0%) hyperlipoproteinemia (HLP), whereas the epsilon 4-carrying patients with IHD were characterized by hypercholesterolemia (type IIb HLP: 42.8%, type IIa HLP: 28.6%). It is concluded that both epsilon 2 and epsilon 4 alleles are more associated with IHD than the epsilon 3 allele.     

Long-term,regular remote ischemic preconditioning improves endothelial function in patients with coronary heart disease

Remote ischemic preconditioning (RIPre) can prevent myocardial injury. The purpose of this study was to assess the beneficial effects of long-term regular RIPre on human arteries. Forty patients scheduled for coronary artery bypass graft (CABG) surgery were assigned randomly to a RIPre group (n=20) or coronary heart disease (CHD) group (n=20). Twenty patients scheduled for mastectomy were enrolled as a control group. RIPre was achieved by occluding arterial blood flow 5 min with a mercury sphygmomanometer followed by a 5-min reperfusion period, and this was repeated 4 times. The RIPre procedure was repeated 3 times a day for 20 days. In all patients, arterial fragments discarded during surgery were collected to evaluate endothelial function by flow-mediated dilation (FMD), CD34⁺ monocyte count, and endothelial nitric oxide synthase (eNOS expression). Phosphorylation levels of STAT-3 and Akt were also assayed to explore the underlying mechanisms. Compared with the CHD group, long-term regular RIPre significantly improved FMD after 20 days (8.5±2.4 vs 4.9±4.2%, P<0.05) and significantly reduced troponin after CABG surgery (0.72±0.31 and 1.64±0.19, P<0.05). RIPre activated STAT-3 and increased CD34⁺ endothelial progenitor cell counts found in arteries. Long-term, regular RIPre improved endothelial function in patients with CHD, possibly due to STAT-3 activation, and this may have led to an increase in endothelial progenitor cells.     

Low density lipoprotein receptor activity in cultured fibroblasts from subjects with or without ischemic heart disease (in the absence of familial hypercholesterolemia)

Fibroblast strains from six subjects with ischemic heart disease (IHDs) were compared to strains from 43 subjects without a history of IHD (non-IHDs), with respect to association (plasma membrane binding plus intracellular accumulation) and degradation of radioiodinated LDL (125I-LDL). The subjects (25 females and 24 males) were selected on the criteria that they were twins (one from each pair), 58-61 years old, and living within 200 km of Oslo. None of them suffered from autosomal, dominant hypercholesterolemia, which is associated with reduced cell surface LDL receptor activity and increased susceptibility to IHD. There was a trend towards lower 125I-LDL association values in strains from IHDs than in strains from non-IHDs (P=0.009). There was a significant negative correlation between, on one hand, serum total cholesterol level and on the other fibroblast association (P=0.03) or degradation (P=0.04) of 125I-LDL. We have previously presented data indicating that fibroblast association of LDL may be determined by alternate genes at one single locus. Together with the present limited data, this raises the possibility that normal genes at the LDL receptor locus may render subjects more or less susceptible to ischemic heart disease.     

Complexity of molecular genetics of dyslipidemia in a family highly susceptible to ischemic heart disease

In a Danish family highly susceptible to ischemic heart disease, hyperlipidemia did not simply cosegregate with a previously undescribed 10 bp deletion in the LDL receptor gene causing heterozygous familial hypercholesterolemia (FH). This mutation, designated as FH DK-4, deletes 10 nucleotides from ex on 4 coding for the third cysteine-rich repeat of the ligand-binding domain. The resulting translational frameshift and stop codon corresponding to amino acid position 181 in the LDL receptor cDNA is predicted to result in a truncated LDL receptor protein. Several family members had hyperlipidemia and early onset of ischemic heart disease not due to the 10 bp deletion, and several family members had unexpectedly high serum lipoprotein(a) contributing to high concentrations of serum LDL cholesterol. The study illustrates important limitations and possibilities of molecular genetic diagnosis.     

Possible approaches to the use of phospholipid preparations as membrane cholesterol receptors

Research Institute of Physicochemical Medicine, Ministry of Health of the RSFSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR Yu. M. Lopukhin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 4, pp. 451–453, April, 1989.