Spontaneous arterial dissection: phenotype and molecular pathogenesis
Arterial dissection (AD) is defined as the longitudinal splitting up of the arterial wall caused by intramural bleeding. It can occur as a spontaneous event in all large and medium sized arteries. The histological hallmark of AD is medial degeneration. Histological investigations, gene expression pr...
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| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2010-06, Vol.67 (11), p.1799-1815 |
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| description | Arterial dissection (AD) is defined as the longitudinal splitting up of the arterial wall caused by intramural bleeding. It can occur as a spontaneous event in all large and medium sized arteries. The histological hallmark of AD is medial degeneration. Histological investigations, gene expression profiling and proteome studies of affected arteries reveal disturbances in many different biological processes including inflammation, proteolytic activity, cell proliferation, apoptosis and smooth muscle cell (SMC) contractile function. Medial degeneration can be caused by various rare dominant Mendelian disorders. Genetic linkage analysis lead to the identification of mutations in different disease-causing genes involved in the biosynthesis of the extracellular matrix (FBN1, COL3A1), in transforming growth factor (TGF) beta signaling (FBN1, TGFBR1, TGFBR2) and in the SMC contractile system (ACTA2, MYH11). Genome wide association studies suggest that the CDKN2A/CDKN2B locus plays a role in the etiology AD and other arterial diseases. |
| doi_str_mv | 10.1007/s00018-010-0276-z |
| format | Article |
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It can occur as a spontaneous event in all large and medium sized arteries. The histological hallmark of AD is medial degeneration. Histological investigations, gene expression profiling and proteome studies of affected arteries reveal disturbances in many different biological processes including inflammation, proteolytic activity, cell proliferation, apoptosis and smooth muscle cell (SMC) contractile function. Medial degeneration can be caused by various rare dominant Mendelian disorders. Genetic linkage analysis lead to the identification of mutations in different disease-causing genes involved in the biosynthesis of the extracellular matrix (FBN1, COL3A1), in transforming growth factor (TGF) beta signaling (FBN1, TGFBR1, TGFBR2) and in the SMC contractile system (ACTA2, MYH11). Genome wide association studies suggest that the CDKN2A/CDKN2B locus plays a role in the etiology AD and other arterial diseases.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-010-0276-z</identifier><identifier>PMID: 20155481</identifier><language>eng</language><publisher>Basel: Basel : SP Birkhäuser Verlag Basel</publisher><subject>Animals ; Aortic disease ; Aortic Dissection - etiology ; Aortic Dissection - genetics ; Aortic Dissection - pathology ; Aortic Dissection - physiopathology ; Arterial dissection ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Biosynthesis ; Cell Biology ; Female ; Gene Expression Profiling ; Genetic Predisposition to Disease ; genetics ; Genotype & phenotype ; Humans ; Life Sciences ; Male ; Matrix metalloproteinase (MMP) ; Medial degeneration ; Models, Cardiovascular ; Molecular biology ; Mutation ; Myocytes, Smooth Muscle - pathology ; Myocytes, Smooth Muscle - physiology ; Pathogenesis ; Peptide Hydrolases - metabolism ; Phenotype ; Review ; Smooth muscle cell (SMC) ; Transforming growth factor (TGF) beta signaling ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - physiology ; Vein & artery diseases</subject><ispartof>Cellular and molecular life sciences : CMLS, 2010-06, Vol.67 (11), p.1799-1815</ispartof><rights>Springer Basel AG 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-2eb91438dd78c5d33c57b24c7489c6413f65575f5b7e3a284e8af9af98ba0663</citedby><cites>FETCH-LOGICAL-c559t-2eb91438dd78c5d33c57b24c7489c6413f65575f5b7e3a284e8af9af98ba0663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11115591/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11115591/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,41487,42556,51318,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20155481$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grond-Ginsbach, Caspar</creatorcontrib><creatorcontrib>Pjontek, Rastislav</creatorcontrib><creatorcontrib>Aksay, Suna Su</creatorcontrib><creatorcontrib>Hyhlik-Dürr, Alexander</creatorcontrib><creatorcontrib>Böckler, Dittmar</creatorcontrib><creatorcontrib>Gross-Weissmann, Marie-Luise</creatorcontrib><title>Spontaneous arterial dissection: phenotype and molecular pathogenesis</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell. Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>Arterial dissection (AD) is defined as the longitudinal splitting up of the arterial wall caused by intramural bleeding. It can occur as a spontaneous event in all large and medium sized arteries. The histological hallmark of AD is medial degeneration. Histological investigations, gene expression profiling and proteome studies of affected arteries reveal disturbances in many different biological processes including inflammation, proteolytic activity, cell proliferation, apoptosis and smooth muscle cell (SMC) contractile function. Medial degeneration can be caused by various rare dominant Mendelian disorders. Genetic linkage analysis lead to the identification of mutations in different disease-causing genes involved in the biosynthesis of the extracellular matrix (FBN1, COL3A1), in transforming growth factor (TGF) beta signaling (FBN1, TGFBR1, TGFBR2) and in the SMC contractile system (ACTA2, MYH11). Genome wide association studies suggest that the CDKN2A/CDKN2B locus plays a role in the etiology AD and other arterial diseases.</description><subject>Animals</subject><subject>Aortic disease</subject><subject>Aortic Dissection - etiology</subject><subject>Aortic Dissection - genetics</subject><subject>Aortic Dissection - pathology</subject><subject>Aortic Dissection - physiopathology</subject><subject>Arterial dissection</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biosynthesis</subject><subject>Cell Biology</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Genetic Predisposition to Disease</subject><subject>genetics</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Matrix metalloproteinase (MMP)</subject><subject>Medial degeneration</subject><subject>Models, Cardiovascular</subject><subject>Molecular biology</subject><subject>Mutation</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>Myocytes, Smooth Muscle - physiology</subject><subject>Pathogenesis</subject><subject>Peptide Hydrolases - metabolism</subject><subject>Phenotype</subject><subject>Review</subject><subject>Smooth muscle cell (SMC)</subject><subject>Transforming growth factor (TGF) beta signaling</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - physiology</subject><subject>Vein & artery diseases</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kU9rFjEQxoNYbK1-AC-6ePG0NZM_m6yXIqVqoeChFbyFbHb2fVP2TdZkV2g_vSn7Wq0HQyAD85tnZvIQ8groCVCq3mdKKeiaAq0pU01994QcgWC0bqmCp_u40ez7IXme802BpWbNM3LISiSFhiNyfjXFMNuAccmVTTMmb8eq9zmjm30MH6ppiyHOtxNWNvTVLo7oltGmarLzNm4wYPb5BTkY7Jjx5f49Jtefzq_PvtSXXz9fnH28rJ2U7Vwz7FoQXPe90k72nDupOiacErp1jQA-NFIqOchOIbdMC9R2aMvVnaVNw4_J6So7Ld0Oe4dhTnY0U_I7m25NtN48zgS_NZv400A5ZQIoCu_2Cin-WDDPZuezw3Fcf8AozjmwRopCvv2HvIlLCmU7w4BL4C3TBYIVcinmnHB4mAWoubfIrBaZYpG5t8jclZrXfy_xUPHbkwKwFcglFTaY_nT-n-qbtWiw0dhN8tl8uyqSvHCCgWz5LzjjpuM</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Grond-Ginsbach, Caspar</creator><creator>Pjontek, Rastislav</creator><creator>Aksay, Suna Su</creator><creator>Hyhlik-Dürr, Alexander</creator><creator>Böckler, Dittmar</creator><creator>Gross-Weissmann, Marie-Luise</creator><general>Basel : SP Birkhäuser Verlag Basel</general><general>SP Birkhäuser Verlag Basel</general><general>Springer Nature B.V</general><scope>FBQ</scope><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</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>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100601</creationdate><title>Spontaneous arterial dissection: phenotype and molecular pathogenesis</title><author>Grond-Ginsbach, Caspar ; Pjontek, Rastislav ; Aksay, Suna Su ; Hyhlik-Dürr, Alexander ; Böckler, Dittmar ; Gross-Weissmann, Marie-Luise</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-2eb91438dd78c5d33c57b24c7489c6413f65575f5b7e3a284e8af9af98ba0663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Aortic disease</topic><topic>Aortic Dissection - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular life sciences : CMLS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grond-Ginsbach, Caspar</au><au>Pjontek, Rastislav</au><au>Aksay, Suna Su</au><au>Hyhlik-Dürr, Alexander</au><au>Böckler, Dittmar</au><au>Gross-Weissmann, Marie-Luise</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Spontaneous arterial dissection: phenotype and molecular pathogenesis</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><stitle>Cell. Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2010-06-01</date><risdate>2010</risdate><volume>67</volume><issue>11</issue><spage>1799</spage><epage>1815</epage><pages>1799-1815</pages><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>Arterial dissection (AD) is defined as the longitudinal splitting up of the arterial wall caused by intramural bleeding. It can occur as a spontaneous event in all large and medium sized arteries. The histological hallmark of AD is medial degeneration. Histological investigations, gene expression profiling and proteome studies of affected arteries reveal disturbances in many different biological processes including inflammation, proteolytic activity, cell proliferation, apoptosis and smooth muscle cell (SMC) contractile function. Medial degeneration can be caused by various rare dominant Mendelian disorders. Genetic linkage analysis lead to the identification of mutations in different disease-causing genes involved in the biosynthesis of the extracellular matrix (FBN1, COL3A1), in transforming growth factor (TGF) beta signaling (FBN1, TGFBR1, TGFBR2) and in the SMC contractile system (ACTA2, MYH11). Genome wide association studies suggest that the CDKN2A/CDKN2B locus plays a role in the etiology AD and other arterial diseases.</abstract><cop>Basel</cop><pub>Basel : SP Birkhäuser Verlag Basel</pub><pmid>20155481</pmid><doi>10.1007/s00018-010-0276-z</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Aortic disease Aortic Dissection - etiology Aortic Dissection - genetics Aortic Dissection - pathology Aortic Dissection - physiopathology Arterial dissection Biochemistry Biomedical and Life Sciences Biomedicine Biosynthesis Cell Biology Female Gene Expression Profiling Genetic Predisposition to Disease genetics Genotype & phenotype Humans Life Sciences Male Matrix metalloproteinase (MMP) Medial degeneration Models, Cardiovascular Molecular biology Mutation Myocytes, Smooth Muscle - pathology Myocytes, Smooth Muscle - physiology Pathogenesis Peptide Hydrolases - metabolism Phenotype Review Smooth muscle cell (SMC) Transforming growth factor (TGF) beta signaling Transforming Growth Factor beta - genetics Transforming Growth Factor beta - physiology Vein & artery diseases |
| title | Spontaneous arterial dissection: phenotype and molecular pathogenesis |
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