<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luo W</submitter><funding>NIEHS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><pagination>42-66</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6939474</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>141(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Sporadic aortic aneurysm and dissection (AAD), caused by progressive aortic smooth muscle cell (SMC) loss and extracellular matrix degradation, is a highly lethal condition. Identifying mechanisms that drive aortic degeneration is a crucial step in developing an effective pharmacologic treatment to prevent disease progression. Recent evidence has indicated that cytosolic DNA and abnormal activation of the cytosolic DNA sensing adaptor STING (stimulator of interferon genes) play a critical role in vascular inflammation and destruction. Here, we examined the involvement of this mechanism in aortic degeneration and sporadic AAD formation.&lt;h4>Methods&lt;/h4>The presence of cytosolic DNA in aortic cells and activation of the STING pathway were examined in aortic tissues from pat</pubmed_abstract><journal>Circulation</journal><pubmed_title>Critical Role of Cytosolic DNA and Its Sensing Adaptor STING in Aortic Degeneration, Dissection, and Rupture.</pubmed_title><pmcid>PMC6939474</pmcid><funding_grant_id>P30 CA016672</funding_grant_id><funding_grant_id>R01 HL118462</funding_grant_id><funding_grant_id>R01 HL131980</funding_grant_id><funding_grant_id>S10 OD025240</funding_grant_id><funding_grant_id>S10 OD018033</funding_grant_id><funding_grant_id>R01 HL127111</funding_grant_id><funding_grant_id>P30 ES030285</funding_grant_id><funding_grant_id>R01 HL130193</funding_grant_id><funding_grant_id>R01 HL123346</funding_grant_id><funding_grant_id>R01 HL143359</funding_grant_id><funding_grant_id>S10 OD023469</funding_grant_id><funding_grant_id>P30 CA125123</funding_grant_id><pubmed_authors>Azares AR</pubmed_authors><pubmed_authors>Coarfa C</pubmed_authors><pubmed_authors>Abe JI</pubmed_authors><pubmed_authors>Rajapakshe K</pubmed_authors><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Shen YH</pubmed_authors><pubmed_authors>Starosolski ZA</pubmed_authors><pubmed_authors>Coselli JS</pubmed_authors><pubmed_authors>Fujiwara K</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Guo J</pubmed_authors><pubmed_authors>Milewicz DM</pubmed_authors><pubmed_authors>Luo W</pubmed_authors><pubmed_authors>Ren P</pubmed_authors><pubmed_authors>LeMaire SA</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Ghaghada KB</pubmed_authors><pubmed_authors>Chen R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Critical Role of Cytosolic DNA and Its Sensing Adaptor STING in Aortic Degeneration, Dissection, and Rupture.</name><description>&lt;h4>Background&lt;/h4>Sporadic aortic aneurysm and dissection (AAD), caused by progressive aortic smooth muscle cell (SMC) loss and extracellular matrix degradation, is a highly lethal condition. Identifying mechanisms that drive aortic degeneration is a crucial step in developing an effective pharmacologic treatment to prevent disease progression. Recent evidence has indicated that cytosolic DNA and abnormal activation of the cytosolic DNA sensing adaptor STING (stimulator of interferon genes) play a critical role in vascular inflammation and destruction. Here, we examined the involvement of this mechanism in aortic degeneration and sporadic AAD formation.&lt;h4>Methods&lt;/h4>The presence of cytosolic DNA in aortic cells and activation of the STING pathway were examined in aortic tissues from pat</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jan</publication><modification>2025-04-22T10:34:49.639Z</modification><creation>2021-02-20T19:14:20Z</creation></dates><accession>S-EPMC6939474</accession><cross_references><pubmed>31887080</pubmed><doi>10.1161/CIRCULATIONAHA.119.041460</doi><doi>10.1161/circulationaha.119.041460</doi></cross_references></HashMap>