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病毒性心肌炎与扩张型心肌病关系的研究进展 总被引:14,自引:0,他引:14
杨英珍 《临床心血管病杂志》1995,(6)
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... 相似文献
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李仲芝 《中国动脉硬化杂志》1995,3(4):323-324
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... 相似文献
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免疫病理与原发性扩张型心肌病 总被引:1,自引:0,他引:1
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… 相似文献
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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。 相似文献
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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。 相似文献
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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。 相似文献
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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. 相似文献
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自噬在心肌缺血再灌注中作用的研究进展 总被引:1,自引:0,他引:1
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。 相似文献
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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. 相似文献
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Alavian SM Ande SR Coombs KM Yeganeh B Davoodpour P Hashemi M Los M Ghavami S 《Journal of viral hepatitis》2011,18(12):821-830
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. 相似文献
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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. 相似文献
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Autophagy in cardiac myocyte homeostasis, aging, and pathology 总被引:8,自引:0,他引:8
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. 相似文献
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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. 相似文献
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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. 相似文献