炎性细胞因子与左心室重构

充血性心力衰竭是临床上高血压病、心肌梗死等多种心脏疾病的最终发展结果，其患病率和死亡率一直居高不下。左心室重构是充血性心力衰竭发展过程中的重要决定因素，许多对左心室重构的研究发现：炎性细胞因子对心肌细胞和细胞外基质发挥较大的作用，引起左心室重构。本文通过综述炎性细胞因子与左心室重构之间的关系，探讨通过抗炎途径纠正左心室重构，治疗充血性心衰的机制和效果。     

致炎性细胞因子在心力衰竭中的病理及临床意义

充血性心力衰竭 (CHF)是心脏疾病死亡的主要原因之一。CHF的病理学改变 ,不仅表现为心肌工作细胞的减少 ,心肌细胞兴奋 收缩耦联异常 ,而且表现为多种细胞因子生成及非特异性炎性反应 ,细胞凋亡和心室重构。本文重点介绍CHF中致炎性细胞因子的病理作用及其临床意义。1　致炎性     

代谢与细胞因子对心力衰竭的影响

本文介绍了多种代谢与细胞因子紊乱对心力衰竭发生发展的影响.发现上述诸种因子对心力衰竭中心室重塑具有促进或拮抗作用,例如血管内皮素、炎性因子、肾上腺髓质素、NO等.近年的研究还显示中医药对心力衰竭过程中代谢与细胞因子具有有利影响,可以作为中西医结合治疗的依据.同时还简介了利用某些代谢与细胞因子对慢性心力衰竭进行定量诊断的探讨.     

脂联素对心力衰竭影响的研究进展

脂联素是一种脂肪源性细胞因子,对心血管系统有保护作用.然而,近年来研究却发现,循环中增高的脂联素是心力衰竭患者死亡的独立预测因子,其机制尚不清楚.脂联素对心力衰竭的作用是否受到某些生物标记物、药物、合并症等诸因素的影响也有待研究.     

高血压与炎症的研究进展

高血压病的发生机制是一个复杂的病理过程。其中,全身动脉血管炎症反应参与高血压的病理生理过程,它是多种炎症细胞、递质、细胞因子共同作用的结果。现综述炎性细胞、炎性细胞因子在高血压发生发展过程中的作用,并介绍高血压的抗炎治疗进展。     

趋化因子CXCL16在心力衰竭发病机制中的研究进展

心力衰竭(HF)是心血管疾病死亡率增加的重要原因,尽管新的治疗方案不断引进,但HF患者的死亡率仍很高.随着研究的进展,人们发现HF的病理生理过程不仅受神经内分泌系统影响,而且与炎症细胞因子的调控密切相关,而趋化因子是炎症发生、发展的过程中重要的促炎细胞因子.在众多趋化因子家族中,CXC亚族是近年来研究的热点,其中CXCL16是既能以分泌又能以膜结合形式存在的趋化因子,在心血管疾病中作用受到越来越多学者的关注,但在HF中却鲜有报道.     

抗炎类药物对射血分数保留性心力衰竭患者心外膜脂肪组织的影响

心外膜脂肪组织在心血管疾病中起着重要作用.近年来研究发现,慢性炎症或代谢紊乱可引起心外膜脂肪组织分泌脂肪因子及游离脂肪酸,进一步导致心功能障碍,最终加快心力衰竭的发展,尤其是射血分数保留性心力衰竭.临床研究证实抗炎类药物(如他汀类药物和抗细胞因子制剂)能降低心外膜脂肪组织厚度,改善炎症状态,有利于降低射血分数保留性心力...     

抗炎症细胞因子在心力衰竭中的治疗进展

充血性心力衰竭是多种心血管疾病所致的一种临床综合征,近年来愈来愈多的研究证实,炎症细胞因子介导的免疫应答在心力衰竭的病理生理过程中起到了重要致病作用.干预此过程已经成为近年来研究的热点.本文总结了目前心力衰竭中抗炎症细胞因子治疗的现状,探讨通过此途径治疗心力衰竭的效果.     

炎性介质和慢性心力衰竭

慢性心力衰竭是一累及心血管系统、骨骼肌、肾脏、神经内分泌和免疫系统的多系统疾病。在最初的心脏损伤或基因序列突变后，神经激素及致炎性细胞因子激活而导致慢性心衰进展。本文对致炎性细胞因子在心衰时的作用和治疗对策作一综述。     

吸入糖皮质激素对哮喘患者Th1/Th2细胞因子网络影响

支气管哮喘(哮喘)是一种慢性气道炎症疾病,多种炎性细胞和炎性介质参与其过程。目前认为T辅助淋巴细胞两个功能性亚群Th1／Th2相关细胞因子在哮喘发病中发挥重要作用。我们对哮喘患者白细胞介素-5(IL-5)、白细胞介素-8(IL-8)r-干扰素(IFN-r)水平进行检测,探讨吸入糖皮质激素对哮喘患者Th1／Th2细胞因子的影响。     

A glossary of circulating cytokines in chronic heart failure

Recent studies have emphasized the importance of biologically active molecules, termed cytokines, in the development and progression of the syndrome of chronic heart failure. This article summarizes a glossary of major cytokines and other cytokine-related inflammatory factors implicated in the pathophysiology of chronic heart failure, describing the source of their synthesis and factors regulating their secretion and analyzing their biologic effects on the cardiovascular system.     

Inflammatory cytokines and nitric oxide in heart failure and potential modulation by vagus nerve stimulation

In heart failure, an inflammatory response may occur. The relationship between inflammatory cytokines, NOS and heart failure progression remains uncertain. Parasympathetic activation can affect heart rate and AV conduction. In heart failure, a relationship between the vagus nerve and the inflammatory response has been proposed. Vagal nerve stimulation can modulate the inflammatory response and affect specific inflammatory mediators including nitric oxide that may be contributory to continued or progressive heart failure. Therefore, vagal nerve stimulation may have beneficial effects that are independent from heart rate or AV conduction in heart failure. Challenges remain regarding the relationship between specific inflammatory markers and heart failure and how to best modulate the cytokines and NOS in patients to achieve beneficial effects. Future studies need to evaluate whether modulating inflammatory cytokines and NOS via vagal nerve stimulation can improve cardiac performance and outcomes in patients with heart failure.     

Systemic inflammatory response following acute myocardial infarction

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI.     

抗细胞因子治疗心力衰竭的研究进展

近年来 ,炎性细胞因子在心力衰竭发展中的作用已成为研究热点。有研究证实 ,抗细胞因子治疗可以减缓心力衰竭进程。因此 ,为了明确炎性细胞因子在心力衰竭病理生理发生机制中的作用 ,就以下几个方面作简要介绍 :炎性细胞因子的生物学特性及其对心脏重塑及心力衰竭发生发展的影响 ,目前抗细胞因子治疗心力衰竭策略的现状。     

Effects of exercise training on inflammatory markers in patients with heart failure

Cardiologists now recognize that the cardio-centric model of heart failure does not sufficiently explain the entire traits particular to chronic heart failure. Evidence accumulates, that many features of the syndrome can be explained by the known biological effects of inflammatory mediators. Indeed, when expressed in experimental models at concentrations commonly observed in heart failure, inflammatory mediators such as tumor necrosis factor-α, interleukin-6, and nitric oxide can produce effects that mimic features of heart failure, including (but not limited to) progressive left-ventricular dysfunction, pulmonary edema, left-ventricular remodeling, and cardiomyopathy. As we witness anti-cytokine therapies and other strategies to avoid an increase in cytokines we have been shown that acute bouts of exercise are associated with an increase in pro-inflammatory cytokines and markers of oxidative stress. As a consequence we have been warned exercise may thus even further contribute to the deterioration of heart failure. However, there are several randomized trials which unanimously document that chronic—as opposed to acute bouts of—exercise does not only lead to a reduction of cytokines and oxidative stress, but that patients dramatically benefit by the increase in maximal oxygen consumption, exercise capacity, quality of life, reduction in hospitalization, morbidity, and mortality. Over the past two decades it has become evident that cytokine research has come to stay and that we will continue to see anti-cytokine treatment strategies for our patients. It is the aim of this review to shed some more light on the most commonly investigated and most relevant cytokines.     

The cytokine network in heart failure: pathogenetic importance and potential therapeutic targets

Accumulating evidence indicates that inflammatory mediators are important in the pathogenesis of chronic heart failure. Several studies have shown raised levels of inflammatory cytokines in patients with congestive heart failure (CHF), in both plasma and circulating leukocytes, as well as in the failing myocardium itself. Importantly, many of the inflammatory cytokines (e.g. tumor necrosis factor-a and interleukin-6) have the potential to negatively influence heart contractility, induce hypertrophy, and promote apoptosis or fibrosis, thereby contributing to the continuous remodeling process in CHF. Traditional cardiovascular drugs seem to have little influence on the cytokine network in CHF patients, and immunomodulatory therapy, in addition to 'optimal' cardiovascular treatment regimens, has emerged as an option. Thus, several small studies with therapy targeted against inflammatory mediators have shown promising effects on functional capacity and myocardial performance. These studies suggest a potential for immunomodulating therapy, in addition to optimal conventional cardiovascular-treatment regimens in CHF patients. However, the results in these small studies will have to be confirmed in larger placebo-controlled mortality studies. More importantly, further research in this area will have to precisely identify the most important components in the immunopathogenesis of chronic heart failure, in order to develop more specific immunomodulating agents in this disorder.     

炎症和心力衰竭

炎症是心血管疾病的重要方面,心力衰竭病人炎症因子常过度表达,其通过影响心肌收缩力,引起心肌肥大,诱导心肌凋亡、纤维化,促进心脏重构等作用促进心力衰竭的发生发展,而且炎症因子预示着心血管不良事件的发生。抗炎将是极有希望的治疗心力衰竭的措施。     

Increased interleukin-13 levels in patients with chronic heart failure

A great number of basic and clinical studies have demonstrated that inflammatory cytokines play an important role in development and progress of heart failure. However, there is limited information about allergic cytokine interleukin-13 (IL-13). The inflammatory responses mediated by allergic cytokines can cause significant morbidity and mortality when they become chronic. Therefore, we elucidated the role of IL-13 in the pathophysiology of chronic heart failure. We measured plasma IL-13 levels by enzyme-linked immunosorbent assay in 110 patients with chronic heart failure and 20 control subjects. Plasma IL-13 levels were increased in heart failure patients, compared with the controls, in association with NYHA functional class. In addition, IL-13 levels were correlated positively with plasma levels of brain natriuretic peptide and C-reactive protein, and negatively with left ventricular ejection fraction. Plasma IL-13 levels may be useful for evaluating disease severity in chronic heart failure.     

Inflammatory biomarkers in heart failure

Multiple lines of evidence support the "cytokine hypothesis," which suggests that inflammation plays an important role in the development and progression of heart failure. Circulating markers of inflammation, such as tumor necrosis factor alpha, interleukin 6, and C-reactive protein, may be useful in establishing the diagnosis, gauging prognosis, and evaluating the response to therapy in patients with heart failure. In addition to their potential as heart failure biomarkers, inflammatory cytokines have been investigated as targets of heart failure therapy. Although results for therapies directed against specific cytokines (such as tumor necrosis factor alpha) have thus far been disappointing, multiple studies continue to address the therapeutic potential of modulating the immune response in heart failure. In this review, the authors analyze available data supporting the use of inflammatory markers both as biomarkers and as potential therapeutic targets.