病毒性心肌炎与扩张型心肌病关系的研究进展

病毒性心肌炎与扩张型心肌病关系的研究进展杨英珍众多实验及临床资料提示病毒性心肌炎（ＶＭＣ）可转化为扩张型心肌病（ＤＣＭ），而将与病毒有关的心肌疾病统称为病毒性心脏病（ＶＨＤ）［１］。至于急性ＶＭＣ后的病毒持续感染，是否通过细胞介导免疫、自身免疫、细胞...     

自噬与脂肪性肝病

自噬（ autophagy）是真核细胞所特有的生命现象,是细胞利用溶酶体降解自身受损的细胞器如线粒体和大分子物质的过程,自噬参与细胞废物的清除、结构的重建、生长与分化,是细胞对不良刺激的一种生存防御机制。近年来,自噬与肝脏疾病的关系已成为医学研究的热点,自噬与肝脏缺血性疾病、肝脏肿瘤的发生、发展,以及与某些先天代谢性肝脏疾病都有着密不可分的关系［1］。同时,自噬在脂肪性肝病的发生发展中也起到了举足轻重的作用。     

细胞自噬与肝脏疾病

自噬又称细胞的自体溶解,是指隔离膜包裹胞质蛋白和细胞器形成自噬体,然后与溶酶体融合成自噬溶酶体并在其中降解的过程。自噬现象普遍存在于大部分真核细胞中,通过对细胞内变性蛋白或受损细胞器进行降解,以维持细胞内物质循环及代谢调节的稳定,在细胞生长、分化、功能执行、自我更新、衰老及死亡中发挥着重要调控功能。     

小儿病毒性心肌炎40例临床分析

小儿病毒性心肌炎４０例临床分析李仲芝（醴陵市人民医院儿科，４１２２００）我院在１９９０年１月～１９９５年４月共收治小儿病毒性心肌炎４０例，按九省市小儿病毒性心肌炎协作组制订的诊治标准［１］，经应用大剂量维生素Ｃ和激素等综合治疗，取得较好疗效，现分析如...     

免疫病理与原发性扩张型心肌病

原发性扩张型心肌病（ＤＣＭ）是一种慢性心肌组织病变,其病因和发病机制至今仍不清楚［１］。目前,ＤＣＭ的发病机制主要有二［２］,即：（１）急性病毒性心肌炎发生后病毒持续性感染;（２）自身免疫病变导致的进行性心肌损害。后者包括细胞免疫和体液免疫的异常［３,４］。Ｌｉｍａｓ［５］认为,自身免疫的异常是由于在病毒的诱导下,心肌细胞抗原暴露,人类白细胞抗原（ＨＬＡ－Ｉ）的异常表达［６］并且将自身抗原信息传递给Ｔ淋巴细胞,引起心肌自身细胞和体液免疫损伤。其中血循环中自身抗心肌抗体的存在于ＤＣＭ的发生和发展过…     

病毒性心肌炎中柯萨奇B3病毒对宿主直接损伤机制的研究进展

病毒性心肌炎是一种威胁人类健康的疾病,肠道病毒为主要病原体,其中柯萨奇B3病毒是最常见的病原体之一。病毒性心肌炎的经典发病机制包括病毒对宿主的直接损伤机制及免疫相关发病机制。随时代改变及技术手段的升级,病毒的直接损伤作用机制中出现许多新进展,他们以病毒蛋白酶、氧化应激、自噬、细胞凋亡及宿主miRNA为中心。在疾病的不同阶段宿主对于病毒的作用往往呈现两面性,本文将对此进行阐释。     

细胞自噬与肝炎病毒感染的相关性研究

自噬(autophagy)又称细胞的自体溶解,是指隔离膜包裹胞浆蛋白和细胞器形成自噬体(autophagosome),然后与溶酶体融合成自噬溶酶体(autolysosome)并在其中降解的过程。自噬现象普遍存在于大部分真核细胞中,通过对细胞内变性蛋白或受损细胞器进行降解,以维持细胞内物质循环及代谢调节的稳定,在细胞生长、分化、功能执行、自我更新、衰老及死亡中发挥着重要调控功能。近期有大量研究表明,细胞自噬与肝炎病毒感染的发生、发展及预后有相关性。本文就自噬发生、演变过程中的分子机制及其与肝炎病毒感染的关系作一概述。     

黄芪在人胚心肌细胞培养中抗柯萨奇B2病毒感染的作用

临床观察发现含有黄芪的中药复方提取剂对病毒性心肌炎患者有一定疗效［１～３］。目前认为柯萨奇Ｂ２（ＣｏｘＢ２）病毒性心肌炎的主要病原。作者通过观察ＣｏｘＢ２型病毒感染人胚心肌细胞后的心肌细胞形态学变化及病毒滴度变化，以进一步研究黄芪治疗病毒性心肌炎的作...     

NOX4在心血管疾病中的研究进展

烟酰胺腺嘌呤二核苷酸磷酸氧化酶(nicotinamide adenine dinucleotide phosphatase oxidase,NOX)家族参与细胞多种活动,如增殖、迁移、凋亡、自噬和衰老,其中NOX4在动脉粥样硬化、高血压、病毒性心肌炎和心力衰竭中表达升高。现对NOX4在心血管疾病中的研究进展进行概述,从而为后续的研究提供一定的理论基础。     

自噬在非小细胞肺癌治疗耐药中的研究进展

非小细胞肺癌是最常见的恶性肿瘤之一,其进展迅速,预后差。大多数进展期的非小细胞肺癌患者在接受放化疗及靶向治疗等过程中因出现耐药现象而影响疗效。细胞自噬是真核细胞内广泛存在的现象,对细胞的生长分化、功能发挥以及死亡具有重要的调节作用。自噬功能失调与非小细胞肺癌的治疗耐药关系密切,因此合理调节自噬可能为非小细胞肺癌治疗提供新的治疗策略。     

自噬在常见心血管疾病中的作用

自噬是细胞利用细胞内溶酶体清除过量或受损的长半衰期蛋白质及细胞器的现象。自噬可通过营养剥夺适应,清除细胞内蛋白质及微细胞器等生理及病理学作用和再利用细胞废物,以维持内环境稳定、参与生长发育和疾病的发生及发展。研究发现,自噬参与了心肌肥厚、心室重构、心肌缺血/再灌注损伤等多种心血管疾病病的理生理过程。本文主要阐述自噬在正常心脏及各种常见心脏疾病中作用的研究进展,并初步探讨可能的治疗新靶点。     

寄生虫感染与宿主细胞自噬相互作用研究进展

自噬是一种真核细胞特有的生命现象,是一种保守的细胞内降解系统。通常所说的自噬是通过双层膜包裹细胞质成分形成自噬体,随后与溶酶体融合,从而降解细胞自身物质的过程。自噬可以由饥饿诱导,也可以由包括寄生虫在内的各种病原体所诱导。当机体感染胞内寄生虫时,宿主细胞可以通过自噬清除寄生虫。然而,寄生虫也进化出自身防御机制,能够利用宿主细胞自噬促进自身发育生长。本文综述了目前国内外关于寄生虫感染与宿主细胞自噬相互影响的研究进展,深入探讨自噬作用对防治寄生虫感染和抗虫药物研发具有重要意义。     

自噬与脂代谢

自噬是细胞清除受损或多余的蛋白质和细胞器的降解过程.最近研究发现,脂滴也是自噬过程的底物之一.在营养状态改变时,自噬能够根据机体需要增加或减少对脂滴的降解,从而起到调节脂代谢的作用.此外,自噬在脂滴形成及脂肪组织分化过程中也发挥重要作用.在细胞水平以自噬为靶点是治疗肥胖、胰岛素抵抗和2型糖尿病的新途径.     

自噬在心肌缺血再灌注中作用的研究进展

自噬是指细胞内的自身物质被溶酶体所降解的过程,为普遍存在的生命现象,是细胞处于饥饿状态时的一种自我保护机制。既往研究表明,在心肌缺血再灌注过程中,自噬被诱导激活,自噬体明显增多。自噬在缺血再灌注中的作用表现出双面性,缺血期主要发挥保护作用,但再灌注时期自噬过度激活则表现出损伤作用,可导致自噬性细胞死亡。自噬具体是如何被激活,怎样发挥其影响作用,至今尚无清楚的答案。本文就自噬在心肌缺血再灌注中作用的研究进展进行综述。     

The Role of Autophagy in Varicella Zoster Virus Infection

Autophagy is an evolutionary conserved cellular process serving to degrade cytosolic organelles or foreign material to maintain cellular homeostasis. Autophagy has also emerged as an important process involved in complex interactions with viral pathogens during infection. It has become apparent that autophagy may have either proviral or antiviral roles, depending on the cellular context and the specific virus. While evidence supports an antiviral role of autophagy during certain herpesvirus infections, numerous examples illustrate how herpesviruses may also evade autophagy pathways or even utilize this process to their own advantage. Here, we review the literature on varicella zoster virus (VZV) and autophagy and describe the mechanisms by which VZV may stimulate autophagy pathways and utilize these to promote cell survival or to support viral egress from cells. We also discuss recent evidence supporting an overall antiviral role of autophagy, particularly in relation to viral infection in neurons. Collectively, these studies suggest complex and sometimes opposing effects of autophagy in the context of VZV infection. Much remains to be understood concerning these virus–host interactions and the impact of autophagy on infections caused by VZV.     

Virus-triggered autophagy in viral hepatitis - possible novel strategies for drug development

Autophagy is a very tightly regulated process that is important in many cellular processes including development, differentiation, survival and homoeostasis. The importance of this process has already been proven in numerous common diseases such as cancer and neurodegenerative disorders. Emerging data indicate that autophagy plays an important role in some liver diseases including liver injury induced by ischaemia reperfusion and alpha-1 antitrypsin Z allele-dependent liver disease. Autophagy may also occur in viral infection, and it may play a crucial role in antimicrobial host defence against pathogens, while supporting cellular homoeostasis processes. Here, the latest findings on the role of autophagy in viral hepatitis B and C infection, which are both serious health threats, will be reviewed.     

Too much or not enough of a good thing — The Janus faces of autophagy in cardiac fuel and protein homeostasis

Cells respond to changes in their environment and in their intracellular milieu by altering specific pathways of protein synthesis and degradation. Autophagy is a highly conserved catabolic process involved in the degradation of long-lived proteins, damaged organelles, and subcellular structures. The process is orchestrated by the autophagy related protein (Atg) to form the double-membrane structure autophagosomes, which then fuse with lysosomes to generate autophagolysosomes where subcellular contents are degraded for a variety of cellular processes. Alterations in autophagy play an important role in diseases including cancer, neurodegenerative diseases, aging, metabolic diseases, inflammation and cardiovascular diseases. In the latter, dysregulated autophagy is speculated to contribute to the onset and development of atherosclerosis, ischemia/reperfusion injury, cardiomyopathy, diabetes mellitus, and hypertension. Autophagy may be both adaptive and beneficial for cell survival, or maladaptive and detrimental for the cell. Basal autophagy plays an essential role in the maintenance of cellular homeostasis whereas excessive autophagy may lead to autophagic cell death. The point and counterpoint discussion highlights adaptive vs. maladaptive autophagy. In this review, we discuss the molecular control of autophagy, focusing particularly on the regulation of physiologic vs. defective autophagy.     

Autophagy in cardiac myocyte homeostasis, aging, and pathology

Autophagy, an intralysosomal degradation of cells' own constituents that includes macro-, micro-, and chaperone-mediated autophagy, plays an important role in the renewal of cardiac myocytes. This cell type is represented by long-lived postmitotic cells with very poor (if any) replacement through differentiation of stem cells. Macroautophagy, the most universal form of autophagy, is responsible for the degradation of various macromolecules and organelles including mitochondria and is activated in response to stress, promoting cell survival. This process is also involved in programmed cell death when injury is irreversible. Even under normal conditions, autophagy is somewhat imperfect, underlying gradual accumulation of defective mitochondria and lipofuscin granules within aging cardiac myocytes. Autophagy is involved in the most important cardiac pathologies including myocardial hypertrophy, cardiomyopathies, and ischemic heart disease, a fact that has led to increasing attention to this process.     

Autophagy in immune cell regulation and dysregulation

Autophagy is an ancient pathway required for cell and tissue homeostasis and differentiation. Initially thought to be a process leading to cell death, autophagy is currently viewed as a beneficial catabolic process that promotes cell survival under starvation conditions by sequestering components of the cytoplasm, including misfolded proteins, protein aggregates, and damaged organelles, and targeting them for lysosome-mediated degradation. In this way, autophagy plays a role in maintaining a balance between degradation and recycling of cellular material. The importance of autophagy is underscored by the fact that malfunctioning of this pathway results in neurodegeneration, cancer, susceptibility to microbial infection, and premature aging. Autophagy occurs in almost all cell types, including immune cells. Recent advances in the field suggest that autophagy plays a central role in regulating the immune system at multiple levels. In this review, we focus on recent developments in the area of autophagy-mediated modulation of immune responses.     

Autophagy as a crosstalk mediator of metabolic organs in regulation of energy metabolism

Autophagy plays an important role in the regulation of cellular homeostasis through elimination of aggregated proteins, damaged organelles, and intracellular pathogens. Autophagy also contributes to the maintenance of energy balance through degradation of energy reserves such as lipids, glycogen, and proteins in the setting of increased energy demand. Recent studies have suggested that autophagy, or its deficiency, is implicated in the pathogenesis of insulin resistance, obesity, and diabetes. These effects of autophagy or its deficiency in regulation of energy metabolism are mediated not only by cell-autonomous effects, such as direct autophagic degradation of energy stores or intracellular organelles (endoplasmic reticulum and mitochondria) but also by non-cell-autonomous effects, such as induction/suppression of secreted factors or changes of sympathetic tone. In the present review, we highlight a recent surge in the research on the autophagy in the regulation of energy homeostasis, with a focus on its role as a mediator for crosstalk between metabolic organs.