运动与衰老、心血管健康相关研究进展

<正>心血管疾病(CVD)是现代社会人口死亡的主要原因,超过90%的CVD发生在中老年人[1,2]。衰老增加CVD的风险,其原因之一是全身血管内皮功能障碍[3]。研究表明,氧化应激和炎症是两个引起血管内皮功能衰老的重要机制。规律的有氧运动对心血管的健康非常有好处,但具体机制尚不清楚,本文重点讨论运动通过调节氧化应激和炎症过程进而改善衰老内皮功能的机制。1血管内皮功能血管内皮是覆盖在血管内表面的单层扁平细胞。血管内     

血管通透性增高发生机制研究进展

<正>正常的血管通透性是维持组织液生成与回流平衡的关键因素。烧伤、休克、脓毒症等严重致病因素及慢性炎症反应、糖尿病、高血压、代谢综合征等慢性致病因素,均可引起血管内皮细胞(VEC)的结构与功能破坏,引起血管通透性增高,成为组织水肿、血液流变性异常、微循环障碍的关键环节,严重影响着疾病的预后与转归〔1〕。本文对血管高通透性发生机制的最新研究进展进行综述。1血管通透性血管内皮屏障是维持血管通透性的重要因素。VEC间不     

中医药保护血管内皮细胞作用机制的研究进展

血管内皮细胞(vascular endothelial cell,VEC)不仅是血流和血管壁之间的机械屏障,而且是高度活化的、功能异常活跃的内分泌、旁分泌及代谢器官,多种理化因素可导致内皮细胞功能障碍,成为血管性疾病产生的关键环节[1],中医药具有明显的保护VEC的作用,现将近年研究概况综述如下.     

中药对血管内皮细胞功能障碍保护作用的研究进展

血管内皮细胞(VEC)不仅是一个机械屏障,而且是人体最大的内分泌器官,VEC的损伤是多种疾病发生、发展的基础.中药在保护、减轻和逆转VEC方面起着重要作用.     

脓毒症血管内皮细胞膜联蛋白A2与钙黏蛋白相互作用研究进展

血管内皮屏障损伤、微循环血管通透性增加是引起脓毒症循环异常的关键病理生理环节,膜联蛋白A2（ANXA2）与血管内皮钙黏蛋白（VE-cadherin）的相互作用在这一过程中扮演了重要角色.Src激酶参与的下游信号转导通路和脓毒症时血管内皮细胞（VEC）损伤密切相关.Src激酶为非受体酪氨酸激酶家族成员,可与ANXA2相互作用.Src介导的酪氨酸磷酸化过程可能是ANXA2调节VE-cadherin的机制,而这一机制可能会加剧脓毒症微循环血管屏障的损伤.本文对脓毒症VEC ANXA2与VE-cadherin相互作用的研究进展作一综述.     

内皮功能紊乱与心血管疾病研究进展

血管内皮细胞 (VEC)为衬贴在血管腔表面的单层扁平细胞。近年的研究表明它不仅起屏障作用 ,还具有重要的内分泌功能 ,参与血管损伤的修复和免疫反应 ,被人们称为体内最大的内分泌和旁分泌器官。由于VEC的解剖位置处于一个易损的功能性界面 ,其功能容易发生紊乱 ,并且与动脉粥样硬化、高血压及心力衰竭等多种疾病的发生和发展有关。对内皮功能紊乱进行药物干预治疗 ,已成为心血管疾病领域的一个新的发展趋势 ,是治疗和预防与其相关疾病的一条途径。近年来在这方面的研究发展较快 ,本文对此作一综述。1　血管内皮细胞的正常功能概述血管内…     

中药对血管内皮细胞功能的影响

通过对中药影响血管内皮细胞（VEC）的屏障、感受、分泌、损伤修复以及肿瘤性增殖等几个方面进行综述,研究中药对VEC的作用,揭示中医药作用于神经内分泌免疫网络（NEIN）的机制.     

血管内皮细胞与动脉粥样硬化的关系

血管内皮细胞 (VEC)是介于血液与血管壁之间的屏障 ,其损伤被认为是动脉粥样硬化 (AS)发病的早期关键性环节。Ross指出 ,AS的发生是由于VEC和平滑肌细胞受各种危险因子如病毒、机械损伤、免疫复合物 ,特别是氧化型低密度脂蛋白 (ox LDL)的损伤 ,而使血管局部产生的一种过度的慢     

急性心肌梗死不同时期血浆一氧化氮及内皮素的变化

近年来,血管内皮细胞(VEC)损伤及功能紊乱与心血管疾病之间的关系日益受到重视,由于VEC在维持血管张力和血流凋节方面发挥重要作用,能阻滞血小板和白细胞的激活,因而其在急性心肌梗死(AMI)发病机制的作用引起人们的关注,本研究观察71例AMI患者血浆内皮素(ET)及一氧化氮(NO)的变化,探讨VEC损伤与AMI的关系。     

血管内皮细胞功能损伤机制的研究进展

血管内皮细胞(VEC)作为血管腔内的一层特化细胞,是血液和组织之间的关键调控界面,因此也成为了多种血管损伤因素的潜在靶点。VEC损伤是多种慢性疾病的共同生理变化,也是包括动脉硬化在内的多种心血管疾病的初始发病机制,其具体机制尚有待进一步阐明。探究VEC损伤的普遍病理机制有助于改善心血管疾病的发展和预后。文章主要就血管活性物质、炎症反应、氧化应激、凝血系统及其他因素等引起VEC损伤的普遍损伤机制进行综述。     

Pathological aging of the vascular endothelium: are endothelial progenitor cells the sentinels of the cardiovascular system?

Aging is associated with vascular endothelial dysfunction, which ultimately leads to atherosclerosis. On the other hand, it is clear that in young patients with risk factors for cardiovascular diseases (CVD), endothelial dysfunction is an early marker of the ongoing atherogenic process. It is therefore tempting to speculate that risk factors for CVD accelerate the aging process. The aging of an endothelial cell (EC) is not chronological but rather dependent on its replication rate. ECs have a finite number of divisions and enter replicative senescence after exhaustion of this potential. Telomere attrition is believed to be responsible for this phenomenon. Upon reaching a critical minimal telomere length, ECs enter a nondividing state of replicative senescence. Recently, endothelial progenitor cells originating from the bone marrow have been isolated from the circulation. They integrate into the endothelial layer of the vessel and contribute to healing, ischemic repair and angiogenesis. A completely new field of investigation is now open. Are endothelial progenitor cells sensitive to the aging process? Do they prevent endothelial dysfunction? Are they the ultimate shield against the damages induced by risk factors for CVD? There are no definite answers to these questions, but the potential of these cells is tremendous and understanding their physiology is essential.     

Telomere attrition in white blood cell correlating with cardiovascular damage.

Aging is a major risk factor for cardiovascular disease. Chronological aging does not always parallel biological aging, but there is no reliable biomarker for the latter. In the present study, we tested the hypothesis that telomere attrition in white blood cells is related to endothelial dysfunction and the extent of atherosclerosis, and thus may serve as a useful marker for biological aging. We evaluated telomere lengths in white blood cells by measuring the mean telomere restriction fragment length (mTRFL), as well as endothelial function by flow mediated dilatation (FMD) in the brachial artery, in patients with various degrees of cardiovascular damage and in normal subjects. Cardiovascular damage was assessed by a cardiovascular damage (CVD) score, with 1 point being given for the presence of each cardiovascular risk factor (hypertension, hyperlipidemia and diabetes) and for each event (angina, myocardial infarction, cerebrovascular event and peripheral vascular disease). Subset analysis of CVD score groups revealed that mTRFL and FMD decreased in the rank order of CVD score. Although mTRFL was inversely correlated with age, telomere index, defined as the ratio of TRFL to TRFL predicted by age, also decreased with increase in CVD score. These results indicate that telomere attrition in white blood cells is more closely associated with endothelial damage and atherosclerosis than is chronological aging, supporting the hypothesis that mTRFL in white blood cells is a useful marker for biological aging of the cardiovascular system.     

Exercise frequency and arterial compliance in non-diabetic and type 1 diabetic individuals.

BACKGROUND: The role of exercise in preventing cardiovascular disease (CVD) has been well documented. To determine whether this benefit could be related to effects on vascular endothelial function and vessel wall elasticity, thereby preserving arterial compliance, we examined the relationship between habitual exercise and arterial compliance as measured by pulse wave analysis. DESIGN: A cross-sectional study of healthy volunteers and patients with type 1 diabetes. METHODS: Non-diabetic individuals not taking cholesterol or blood pressure-lowering medication (n=176) and patients with type 1 diabetes (n=105), aged 17-70 years, were recruited. Small and large artery compliance and other haemodynamic variables were measured using the PulseWave CR-2000 cardiovascular profiling system. A questionnaire was completed to assess the frequency of physical activity. RESULTS: In multivariate analysis, undertaking three or more episodes of vigorous activity per week was associated with having a 1 unit greater small artery compliance, independent of age, sex, height, diabetes status and blood pressure. The effect was especially marked in non-diabetic women. CONCLUSIONS: The results support other findings that regular physical activity protects against CVD, through the preservation of vascular compliance.     

VEGF对血管内皮细胞损伤的拮抗作用及作用机制

冻结性冷损伤是以组织冻结再融化过程的病理改变为基础的损伤。已经证实,血管内皮细胞（VECs）除有屏障和膜转运功能外,还具有内分泌功能,主动参与了多种生命活动,对维持体内环境的平衡与稳定具有重要作用。冻伤过程中VECs的损伤,可促进微循环血栓形成造成微循环障碍;待到复温后,血液恢复流动又可导致不可逆的再灌注损伤。因此,减轻内皮细胞损伤,可以减少微循环血栓形成,从而减轻再灌注对机体造成的损伤。血管内皮细胞生长因子（VEGF）作为重要的血管生长因子,在冻伤时对VECs损伤具有拮抗作用,可通过促进血管再生、抗血栓形成、抑制血管平滑肌过度生长及抗炎的作用等实现的对血管的保护作用,为临床防治冻伤提供了新的思路。     

The eye, the mirror of the heart.

The major health economical burden of cardiovascular disease(CVD) is leading to a swift move from treatment of CVD to diagnosisof early CVD in asymptomatic people. Primary prevention of CVDhas been aimed at risk factor identification and treatment,without efforts to document early CVD. It is well recognized that vascular changes, including atherosclerosis,begin early in life as a silent, asymptomatic disease process.Therefore, identification of early vascular abnormalities inasymptomatic subjects may help identify asymptomatic individualsat risk, before blood pressure is elevated above an ‘arbitrary’level that we currently identify as hypertension.¹ These vascularparameters     

Nuevos mecanismos implicados en el desarrollo de la enfermedad cardiovascular en la enfermedad renal crónica

Chronic kidney disease (CKD) is a pathology with a high worldwide incidence and an upward trend affecting the elderly. When CKD is very advanced, the use of renal replacement therapies is required to prolong its life (dialysis or kidney transplantation). Although dialysis improves many complications of CKD, the disease does not reverse completely. These patients present an increase in oxidative stress, chronic inflammation and the release of extracellular vesicles (EVs), which cause endothelial damage and the development of different cardiovascular diseases (CVD). CKD patients develop premature diseases associated with advanced age, such as CVD. EVs play an essential role in developing CVD in patients with CKD since their number increases in plasma and their content is modified. The EVs of patients with CKD cause endothelial dysfunction, senescence and vascular calcification. In addition, miRNAs free or transported in EVs together with other components carried in these EVs promote endothelial dysfunction, thrombotic and vascular calcification in CKD, among other effects. This review describes the classic factors and focuses on the role of new mechanisms involved in the development of CVD associated with CKD, emphasizing the role of EVs in the development of cardiovascular pathologies in the context of CKD. Moreover, the review summarized the EVs’ role as diagnostic and therapeutic tools, acting on EV release or content to avoid the development of CVD in CKD patients.     

Vascular consequences of menopause and hormone therapy: importance of timing of treatment and type of estrogen

Premenopausal women have a lower risk for cardiovascular events, and mortality due to coronary vascular disease (CVD) in premenopausal women is rare. These facts suggest that endogenous estrogens, such as estradiol, protect the cardiovascular system, and several observational studies and a few small clinical studies conducted in healthy and younger postmenopausal women support this hypothesis. In contrast, two large randomized clinical trials (RCTs), using conjugated equine estrogens and conducted in older women with established CVD or without overt CVD, failed to demonstrate protection against CVD by exogenous estrogens. These divergent findings have resulted in confusion with regard to the association between estrogen deficiency and CVD in postmenopausal women. In order to reconcile these contradictory findings, it is necessary to examine the pathophysiology associated with age-dependent changes within the vessel wall and to compare the pharmacology of different types of estrogens. Understanding age-dependent changes in vascular pathology and the pharmacology of different estrogens may facilitate the development of therapeutic strategies for hormone replacement therapy (HRT) that would be effective in delaying vascular remodeling leading to CVD following menopause. In this review we provide an overview of the impact of menopause and estrogen deficiency on vascular remodeling and emphasize the importance of timing and type of estrogen to achieve maximum benefits with regard to reducing the risk of CVD.     

A Clinical Perspective: Contribution of Dysfunctional Perivascular Adipose Tissue (PVAT) to Cardiovascular Risk

Perivascular adipose tissue (PVAT) is now recognized as an important paracrine organ influencing the homeostasis of the vessel wall, regional blood flow and peripheral arterial resistance. There is remarkable phenotypic variability and plasticity of PVAT among various vascular beds, exhibiting phenotypes from white to brown and beige adipocytes. PVAT dysfunction is characterized by disturbed secretion of various adipokines, which, together with endothelial dysfunction, contribute to hypertension and cardiovascular disease (CVD). This brief review describes our current knowledge on PVAT in health and cardiovascular disease, with a special focus on different phenotypes and signaling pathways in adipocytes of PVAT associated with hypertension, obesity and cardiovascular disorders.     

Endothelial-dependent mechanisms of leukocyte recruitment to the vascular wall

Inflammation is a fundamental process that protects organisms by removing or neutralizing injurious agents. A key event in the inflammatory response is the localized recruitment of various leukocyte subsets. Here we address the cellular and regulatory mechanisms of leukocyte recruitment to the vessel wall in cardiovascular disease and discuss our evolving understanding of the role of the vascular endothelium in this process. The vascular endothelium is the continuous single-cell lining of the cardiovascular system that forms a critical interface between the blood and its components on one side and the tissues and organs on the other. It is heterogeneous and has many synthetic and metabolic functions including secretion of platelet-derived growth factor, von Willebrand factor, prostacyclin, NO, endothelin-1, and chemokines and the expression of adhesion molecules. It also acts as a nonthrombogenic and selective permeable barrier. Endothelial cells also interact closely with the extracellular matrix and with adjacent cells including pericytes and smooth muscle cells within the vessel wall. A central question in vascular biology is the role of the endothelium in the initiation of inflammatory response, the extent of its "molecular conversations" with recruited leukocytes, and its influence on the extent and/or outcome of this response.