Role of autophagy in advanced atherosclerosis
Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective...
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| Veröffentlicht in: | Molecular medicine reports 2017-05, Vol.15 (5), p.2903-2908 |
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| creator | Zhu, Yu-Ning Fan, Wen-Jing Zhang, Chi Guo, Fang Li, Wei Wang, Yu-Fei Jiang, Zhi-Sheng Qu, Shun-Lin |
| description | Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self-feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self-renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases. |
| doi_str_mv | 10.3892/mmr.2017.6403 |
| format | Article |
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Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self-feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self-renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6403</identifier><identifier>PMID: 28350050</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Arteriosclerosis ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Atherosclerosis ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Autophagy ; Autophagy (Cytology) ; Cardiovascular disease ; Cardiovascular diseases ; Cardiovascular system ; Care and treatment ; Cell survival ; Development and progression ; Health aspects ; Homeostasis ; Humans ; Inflammation ; Kinases ; Lipids ; Lysosomal-Associated Membrane Protein 2 - metabolism ; Macrophages ; Macrophages - immunology ; Macrophages - metabolism ; Mammals ; Metabolism ; molecular mechanism ; Morbidity ; Myocardial infarction ; Organelles ; Oxidative stress ; Phagocytosis ; Protein Phosphatase 2C - metabolism ; Proteins ; Rodents ; Severity of Illness Index ; Stem cells ; TOR Serine-Threonine Kinases - metabolism ; treatment ; vascular ; Vascular diseases ; Yeast</subject><ispartof>Molecular medicine reports, 2017-05, Vol.15 (5), p.2903-2908</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-4151dfe434f05d431755a3bcab6ec2a2a23f130a36e876cb330ba55d24de03263</citedby><cites>FETCH-LOGICAL-c525t-4151dfe434f05d431755a3bcab6ec2a2a23f130a36e876cb330ba55d24de03263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5569,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28350050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Yu-Ning</creatorcontrib><creatorcontrib>Fan, Wen-Jing</creatorcontrib><creatorcontrib>Zhang, Chi</creatorcontrib><creatorcontrib>Guo, Fang</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Wang, Yu-Fei</creatorcontrib><creatorcontrib>Jiang, Zhi-Sheng</creatorcontrib><creatorcontrib>Qu, Shun-Lin</creatorcontrib><title>Role of autophagy in advanced atherosclerosis</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self-feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self-renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases.</description><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>Autophagy</subject><subject>Autophagy (Cytology)</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular system</subject><subject>Care and treatment</subject><subject>Cell survival</subject><subject>Development and progression</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Lysosomal-Associated Membrane Protein 2 - metabolism</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Mammals</subject><subject>Metabolism</subject><subject>molecular mechanism</subject><subject>Morbidity</subject><subject>Myocardial infarction</subject><subject>Organelles</subject><subject>Oxidative stress</subject><subject>Phagocytosis</subject><subject>Protein Phosphatase 2C - metabolism</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Severity of Illness Index</subject><subject>Stem cells</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>treatment</subject><subject>vascular</subject><subject>Vascular diseases</subject><subject>Yeast</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc9LwzAUx4Mobk6PXqXgQS-tL0nTNscx_AUDQfQc0iTdOtqmNq2w_96UzYkiD5IQPu-bRz4IXWKIaMbJXV13EQGcRkkM9AhNccpxSAHi4_2ZcJ5O0JlzG4CEEcZP0YRklAEwmKLw1VYmsEUgh962a7naBmUTSP0pG2V0IPu16axT1biW7hydFLJy5mK_z9D7w_3b4ilcvjw-L-bLUPkH-jDGDOvCxDQugOmY4pQxSXMl88QoIn3RAlOQNDFZmqicUsglY5rE2gAlCZ2h211u29mPwbhe1KVTpqpkY-zgBM4ynKaEsBG9_oNu7NA1fjqBeUISwCTFP9RKVkaUTWH7TqoxVMxjzjjlFIOnon8oX9rUpbKNKUp__6sh3DUo_z2uM4Vou7KW3VZgEKMe4fWIUY8Y9Xj-aj_skNdGH-hvHx642QGulY0utXUHxieFmIXAvFEf9QWmjpQx</recordid><startdate>20170501</startdate><enddate>20170501</enddate><creator>Zhu, Yu-Ning</creator><creator>Fan, Wen-Jing</creator><creator>Zhang, Chi</creator><creator>Guo, Fang</creator><creator>Li, Wei</creator><creator>Wang, Yu-Fei</creator><creator>Jiang, Zhi-Sheng</creator><creator>Qu, Shun-Lin</creator><general>D.A. 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metabolism</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>Autophagy</topic><topic>Autophagy (Cytology)</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular system</topic><topic>Care and treatment</topic><topic>Cell survival</topic><topic>Development and progression</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Lipids</topic><topic>Lysosomal-Associated Membrane Protein 2 - metabolism</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Mammals</topic><topic>Metabolism</topic><topic>molecular mechanism</topic><topic>Morbidity</topic><topic>Myocardial infarction</topic><topic>Organelles</topic><topic>Oxidative stress</topic><topic>Phagocytosis</topic><topic>Protein Phosphatase 2C - metabolism</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Severity of Illness Index</topic><topic>Stem cells</topic><topic>TOR Serine-Threonine Kinases - 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Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Yu-Ning</au><au>Fan, Wen-Jing</au><au>Zhang, Chi</au><au>Guo, Fang</au><au>Li, Wei</au><au>Wang, Yu-Fei</au><au>Jiang, Zhi-Sheng</au><au>Qu, Shun-Lin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of autophagy in advanced atherosclerosis</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-05-01</date><risdate>2017</risdate><volume>15</volume><issue>5</issue><spage>2903</spage><epage>2908</epage><pages>2903-2908</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self-feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self-renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28350050</pmid><doi>10.3892/mmr.2017.6403</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Apoptosis Arteriosclerosis Ataxia Telangiectasia Mutated Proteins - metabolism Atherosclerosis Atherosclerosis - metabolism Atherosclerosis - pathology Autophagy Autophagy (Cytology) Cardiovascular disease Cardiovascular diseases Cardiovascular system Care and treatment Cell survival Development and progression Health aspects Homeostasis Humans Inflammation Kinases Lipids Lysosomal-Associated Membrane Protein 2 - metabolism Macrophages Macrophages - immunology Macrophages - metabolism Mammals Metabolism molecular mechanism Morbidity Myocardial infarction Organelles Oxidative stress Phagocytosis Protein Phosphatase 2C - metabolism Proteins Rodents Severity of Illness Index Stem cells TOR Serine-Threonine Kinases - metabolism treatment vascular Vascular diseases Yeast |
| title | Role of autophagy in advanced atherosclerosis |
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