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<title cf:type="text"><![CDATA[Progress in Biochemistry and Biophysics -->Special Topic: Cell Autophagy]]></title>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Editorial: Autophagy and diseases]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120139]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[自噬是细胞的一个重要生物学功能。细胞通过对自噬底物的识别、自噬囊泡的形成，再经过与溶酶体的融合，清除老化细胞器以及降解长周期蛋白和异常积聚蛋白。因此，自噬在蛋白质的代谢、细胞器更新以及组织发育中有着重要作用，其功能调控直接参与了机体对细胞稳态的维持和对疾病的抵抗。目前已有大量研究表明，自噬与疾病的发生密切相关，如心血管病、肿瘤、炎症和免疫以及神经退行性疾病等。近年来，自噬研究得到了国内外科学家的广泛重视，研究论文的数量直线上升。科技部和国家自然科学基金委均已资助相关课题，这进一步促进了我国在自噬研究领域的发展。我国科学家在自噬的机制和疾病关系研究中也取得了重大进展，许多研究成果已经走在世界前沿。本刊对自噬这一研究领域一直十分关注，为促进对该领域现状及发展的了解，本期汇集了6 篇述评和1 篇研究论文，作为自噬研究专题发表，以飨读者。<br>
本专题主要对自噬与一些相关疾病关系的现状和发展进行了评述，并对自噬研究方法学和基本机制也进行了综述，同时报道了在果蝇脊髓小脑变性3型动物模型中开展的关于自噬与Sir2发挥神经保护作用相关性的研究，反映了目前自噬研究的一个侧面。马泰等主要综述了目前自噬研究的技术和方法进展，评价了自噬的评估指标和这些自噬方法学的应用，提供了一个自噬方法学上的基础交流。吴葩等介绍了PI3K复合物中各组分蛋白与细胞自噬的关系，详细阐述了该通路在细胞自噬调节中的最新研究进展，为这一信号通路研究提供了信息。何云凌等很好地总结了低氧环境诱导线粒体自噬发生的相关分子机制，对参与调节线粒体自噬的重要蛋白进行了系统的描述，为目前人们普遍关注的线粒体自噬与疾病的关系提供了前沿资料。谢凤等对心脏疾病状态下细胞自噬的发生、发展及其对心脏疾病的影响进行了详细的论述，有助于研究者从自噬的角度来探讨心脏疾病的发生发展及其机制。林小龙等围绕当前热点问题对自噬与血管内皮细胞的关系作了描述，介绍了血管内皮细胞在各种药物刺激以及相关蛋白质过表达情况下对于自噬的反应以及所引起的下游应答，探讨了自噬与血管疾病发病的相互关系。向波等介绍了细胞自噬与肿瘤的发生发展的关系，描述了炎症-自噬-肿瘤的相关性以及自噬可能的抑瘤机制。曾爱源等利用果蝇的遗传性脊髓小脑变性3 型模型，研究了Sir2在自噬存在情况下对转基因果蝇的神经保护作用，并发现在自噬抑制后Sir2的保护作用明显减弱，揭示了Sir2通过自噬保护神经元、减缓神经变性蛋白损伤的作用机制。<br>
本刊欢迎和期待更多、更好的有关自噬研究的来稿，以更广泛和深入地促进我国自噬研究领域的发展和学术交流。]]></description>
<pubDate>2012/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[WANG Guang-Hui]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Guang-Hui</atom:name>
</atom:author>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Review: Methods for Autophagy Detection]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120010]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Autophagy extensively participate in physiological and pathological processes, and has been focused by contemporary biomedicine scientists in recent years. Transmission electron microscopy, immunofluorescence and immunoblotting techniques were common used in detection of autophagy. Deeper research needs more accurate detection of autophagy. Dysfunction of autophagy involves formation and degeneration of autophosome, accordingly, accurate and comprehensive evaluation of autophagy includes autophosome detection, as well as the fluency of autophagic degeneration, i.e. autophagic flux assay. Additionally, artificial up- or down-regulation of autophagy by drugs or gene interferences in <i>in vitro</i> or <i>in vivo</i> models has also been considered as important part of autophagy analysis. Any method currently used alone may not been as evidence of autophagy. More careful attention should be paid on results of any assays of autophagy, especially DO NOT interpret "increase or decrease of autophosome" (also "up- or down-expression of autophagy-related proteins") as "enhancement or attenuation of autophagic function".]]></description>
<pubDate>2012/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[MA Tai,SUN Guo-Ping and LI Jia-Bin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MA Tai,SUN Guo-Ping and LI Jia-Bin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120010]]></guid><cfi:id>7</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Review: Advances in Relationship Between Class Ⅲ PI3K Complex and Autophagy]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110387]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Class Ⅲ phosphoinositide 3-kinase (class Ⅲ PI3K), which specifically phosphorylate PtdIns to generate PtdIns3P, plays a vital role in autophagy and vacuolar sorting pathways by forming Class Ⅲ PI3K(PI3KC3) complexes with a variety of regulatory proteins. Proteins that compose PI3KC3 complex, namely, PI3K, p150, Beclin 1, ATG14L, UVRAG, Bif-1 and Rubicon are conserved in evolution. In addition, neurodevelopment, situs inversus totalis and development of tumor are found to closely related to these members.]]></description>
<pubDate>2011/12/20 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[WU Pa and XU Cai-Min]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Pa and XU Cai-Min</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110387]]></guid><cfi:id>6</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Review: The Role of Mitophagy in Hypoxic Adaptation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110191]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Hypoxia is a representative stress environment, under which cell energy and oxidative metabolism change a lot. Among the product of metabolism, reactive oxygen species (ROS) which generate from mitochondria under hypoxia seriously threaten cell survive. Mitophagy was recently found as an adaptive metabolic response to hypoxia. Cell induces mitophagy by the pathway mediated by BNIP3/BNIP3L and Beclin-1 that are activated by up-regulation of HIF-1 under hypoxia, then reduces the production of ROS, and ultimately promotes cell survival. This process leads to the adaptation of organism to hypoxia. In this paper, we will overview the role and the mechanism of mitophagy in adaptation to hypoxia.]]></description>
<pubDate>2011/11/23 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[HE Yun-Ling,WU Li-Ying,ZHU Ling-Ling and FAN Ming]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HE Yun-Ling,WU Li-Ying,ZHU Ling-Ling and FAN Ming</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110191]]></guid><cfi:id>5</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Review: The Progress of Autophagy Involved in Heart Disease]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120088]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Autophagy is a process in which damaged, modified or aging proteins and organelles are transported to the lysosome/vacuole for degradation. Autophagy is not only a widespread normal physiological process, but also a cell defense mechanism to adverse environment, involved in the pathological process of diseases. The normal level of autophagy can protect cells from environmental stimuli, however, continued excessive or insufficient autophagy could lead to disease. In the heart, myocardial autophagy plays a vital role to maintain myocardial function, but dysfunctional autophagy contributes to a diverse set of heart diseases, such as Danon disease. Multiple forms of cardiovascular stress can increase autophagic activity in cardiomyocytes, including chronic ischemia, reperfusion injury and Chronic hypoxia. The function of autophagy in these conditions is poorly understood: Does it serve a pro-survival function or contribute to disease pathogenesis, cell death, or both? Heart disease is the abnormal myocardia function when to produce a variety of pathological state. In the state of disease, cardiac autophagy degree will change, related to the occurrence and development of disease. As in Hypertrophic cardiomyopathy process, cell autophagy is reduced and aggravate myocardial hypertrophy. In heart failure process, autophagy increases can lead to cell death; And in myocardial infarction process, autophagy is enhanced and reduce the infarction area. But the real role of autophagy in the myocardium depending on the level of autophagic activation and the context in which it is induced. Currently, more and more people begin to pay close attention to the relationship between drugs and autophagy regulation, particularly on antitumor drugs and cardiovascular drugs. In addition, there are reports of estrogen receptor antagonists tamoxifen and vitamins also has a regulatory role for autophagy. To research of the relationship between autophagy and heart disease, and drugs on the regulation of autophagy will benefit for the occurrence and development of heart disease, and explore a new mechanism of drug treatment from the autophagy perspectives.]]></description>
<pubDate>2012/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[XIE Feng,LIU Wei and CHEN Lin-Xi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>XIE Feng,LIU Wei and CHEN Lin-Xi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120088]]></guid><cfi:id>4</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Review: The Factors Influence Vascular Endothelial Cells of Autophagy and Related Mechanism]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120098]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Autophagy plays critical role in maintaining the cell homeostasis, organelle turnover and nutrient recycling in physiological condition. Autophagy is consist in the body's physiological and pathological process. It has protection and repairing role at basic autophagy level, but over-autophagy would lead to injury and apoptosis. In the past years, major studies are focussing on cancer cell autophagy, and only a few studies concerning about normal cells. Vascular endothelial cells as one of the most active cells in the human body, many cardioascular disease were bound up with vascular endothelial cells (VECs) function change. This review summarizes influence factors on vascular endothelial cells autophagy.]]></description>
<pubDate>2012/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[LIN Xiao-Long,MA Xiao-Feng,LI Shuang,ZHAO Yue and WANG Zuo]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LIN Xiao-Long,MA Xiao-Feng,LI Shuang,ZHAO Yue and WANG Zuo</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120098]]></guid><cfi:id>3</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Review: Progress on Role of Autophagy in Cancer]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110555]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Autophagy is an evolutionarily conserved catabolic process crucial for development, differentiation, survival, and homeostasis. However, if it proceeds to completion, autophagy can lead to cell death. Changes in macroautophagy activity have been described in cancer cells and in solid tumors, and inhibition of macroautophagy promotes tumorigenesis. The review focuses on the importance of autophagy in tumour development and cancer therapy. We summarize what is currently known about autophagy, and discuss its role in cell death and survival. We discuss possible mechanisms underlying the anti-tumor activity of autophagy. We also discuss the effect of autophagy modulation in cancer therapy.]]></description>
<pubDate>2012/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[XIANG Bo,YI Mei,LI Xiao-Ling and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>XIANG Bo,YI Mei,LI Xiao-Ling and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110555]]></guid><cfi:id>2</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Research Paper: The Neuro-protective Role of Sir2 in The Process of Neuro-degeneration of The SCA3/MJD Model Flies is Dependent on Autophagy Function]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110367]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[To confer the influence of Sir2 on pathogenesis of SCA3/MJD. GMR-GAL4 and Nrv2-GAL4 system SCA3/MJD transgenic <i>Drosophila</i> models were constructed by using the promoter GMR-GAL4 and Nrv2-GAL4 which drive target selective gene expression in cells of the developing eyes and motor neurons, respectively. Then, Sir2 protein was overexpressed in SCA3/MJD transgenic <i>Drosophila</i> models by genetic methods with or without in a background of RNAi knockdown of <i>Atg7</i>. Overexpression of endogenous <i>Drosophila</i> Sir2 not only notably suppresses the neurotoxicity of MJDtr-Q78 protein, but also significantly improves the movement ability of flies. Moreover, RNAi knockdown of <i>Atg7</i> significantly Sir2's protection against SCA3/MJD <i>Drosophila</i>. We confirmed that overexpression of Sir2 could protect SCA3/MJD <i>Drosophila</i> models, and the protection role of Sir2 on SCA3/MJD <i>Drosophila</i> models is autophagy-dependent.]]></description>
<pubDate>2011/9/27 0:00:00</pubDate>
<category><![CDATA[Special Topic: Cell Autophagy]]></category>
<author><![CDATA[ZENG Ai-Yuan,ZHU Jing-Lei,HONG Kang-Kang,ZHANG Zhuo-Hua,DUAN Ran-Hui,SUN Li,LIU Cheng-Wei,WEI Xiao-Li,WEI Li-Li,CHEN Mei-Ling,LIN Xiao-Hui,CHEN Wei and lI Qing-Hua]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZENG Ai-Yuan,ZHU Jing-Lei,HONG Kang-Kang,ZHANG Zhuo-Hua,DUAN Ran-Hui,SUN Li,LIU Cheng-Wei,WEI Xiao-Li,WEI Li-Li,CHEN Mei-Ling,LIN Xiao-Hui,CHEN Wei and lI Qing-Hua</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110367]]></guid><cfi:id>1</cfi:id><cfi:read>true</cfi:read></item>
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