Atherosclerosis
Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosc...
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| Veröffentlicht in: | Nature (London) 2000-09, Vol.407 (6801), p.233-241 |
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| description | Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis. |
| doi_str_mv | 10.1038/35025203 |
| format | Article |
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In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/35025203</identifier><identifier>PMID: 11001066</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Animals ; Arteriosclerosis - diagnosis ; Arteriosclerosis - drug therapy ; Arteriosclerosis - etiology ; Arteriosclerosis - genetics ; Arteriosclerosis - pathology ; Cardiovascular disease ; Cardiovascular diseases ; Cholesterol ; Coronary Disease - etiology ; Genetics ; Humans ; Medical research ; Metabolism ; Risk Assessment ; Risk factors ; Stroke ; Thromboembolism</subject><ispartof>Nature (London), 2000-09, Vol.407 (6801), p.233-241</ispartof><rights>COPYRIGHT 2000 Nature Publishing Group</rights><rights>Copyright Macmillan Journals Ltd. 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In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis.</description><subject>Animals</subject><subject>Arteriosclerosis - diagnosis</subject><subject>Arteriosclerosis - drug therapy</subject><subject>Arteriosclerosis - etiology</subject><subject>Arteriosclerosis - genetics</subject><subject>Arteriosclerosis - pathology</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cholesterol</subject><subject>Coronary Disease - etiology</subject><subject>Genetics</subject><subject>Humans</subject><subject>Medical research</subject><subject>Metabolism</subject><subject>Risk Assessment</subject><subject>Risk factors</subject><subject>Stroke</subject><subject>Thromboembolism</subject><issn>0028-0836</issn><issn>1476-4687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkV1LwzAUhoMobk7RX-CFV3rRefLRpL0RxvBjMBD8uA5pc7p1bO3WtKL_3pTNzcEInMDJk4fDeQm5otCnwKN7HgILGfAj0qVCyUDISB2TLgCLAoi47JAz52YAEFIlTkmHUgAKUnbJ5aCeYlW6dN7W3J2Tk8zMHV5s7h75fHr8GL4E49fn0XAwDtKQhXWQMIMGLbPSxpaiUCi5ZCrhNg5liFYpAYpazpIkUxCDQq7iLOYikYk1MeM98rD2LptkgTbFoq7MXC-rfGGqH12aXO-_FPlUT8ovzSImGWsFNxtBVa4adLWelU1V-Jk1AyEiwVULBWtoYuao8yIrvSudYIFeWRaY5b49oFEEUvmyk-7x6TJf6f9Q_wDkj8VFnh603u198EyN3_XENM7p0fvbPnu7ZlMfh6sw266Egm6z1n9Ze_T6_wp34CbcHVCYuqlwC2wNv15HqN8</recordid><startdate>20000914</startdate><enddate>20000914</enddate><creator>Lusis, Aldons J</creator><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7ST</scope><scope>7T5</scope><scope>7TG</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PCBAR</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>R05</scope><scope>RC3</scope><scope>S0X</scope><scope>SOI</scope><scope>5PM</scope></search><sort><creationdate>20000914</creationdate><title>Atherosclerosis</title><author>Lusis, Aldons J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-b2aeaed2d6d9d1e47e63627b3d9565ed774071d32bbf70907e379f934b6bda923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Arteriosclerosis - 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In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>11001066</pmid><doi>10.1038/35025203</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature (London), 2000-09, Vol.407 (6801), p.233-241 |
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| source | MEDLINE; Nature; Alma/SFX Local Collection |
| subjects | Animals Arteriosclerosis - diagnosis Arteriosclerosis - drug therapy Arteriosclerosis - etiology Arteriosclerosis - genetics Arteriosclerosis - pathology Cardiovascular disease Cardiovascular diseases Cholesterol Coronary Disease - etiology Genetics Humans Medical research Metabolism Risk Assessment Risk factors Stroke Thromboembolism |
| title | Atherosclerosis |
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