<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xu X</submitter><funding>National Key Scientific Instrument and Equipment Development Projects of China</funding><funding>Guangxi Talent Highland of Preservation and Deep Processing Research in Fruit and Vegetables (CN)</funding><funding>Guangxi Talent Highland of Preservation and Deep Processing Research in Fruit and Vegetables</funding><funding>National Natural Science Foundation of China</funding><funding>National Key Scientific Instrument and Equipment Development Projects of China (CN)</funding><funding>Beijing Science and Technology Planning Project</funding><pagination>119</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8140477</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>18(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Cerebral ischemia-reperfusion (I/R) injury is a major cause of early complications and unfavorable outcomes after endovascular thrombectomy (EVT) therapy in patients with acute ischemic stroke (AIS). Recent studies indicate that modulating microglia/macrophage polarization and subsequent inflammatory response may be a potential adjunct therapy to recanalization. Annexin A1 (ANXA1) exerts potent anti-inflammatory and pro-resolving properties in models of cerebral I/R injury. However, whether ANXA1 modulates post-I/R-induced microglia/macrophage polarization has not yet been fully elucidated.&lt;h4>Methods&lt;/h4>We retrospectively collected blood samples from AIS patients who underwent successful recanalization by EVT and analyzed ANXA1 levels longitudinally before and after EV</pubmed_abstract><journal>Journal of neuroinflammation</journal><pubmed_title>Annexin A1 protects against cerebral ischemia-reperfusion injury by modulating microglia/macrophage polarization via FPR2/ALX-dependent AMPK-mTOR pathway.</pubmed_title><pmcid>PMC8140477</pmcid><funding_grant_id>81671380</funding_grant_id><funding_grant_id>2016YFC1301703</funding_grant_id><funding_grant_id>D161100003816002</funding_grant_id><funding_grant_id>201920200501</funding_grant_id><funding_grant_id>81801231</funding_grant_id><funding_grant_id>82001317</funding_grant_id><pubmed_authors>Jiao L</pubmed_authors><pubmed_authors>Hao J</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Wang D</pubmed_authors><pubmed_authors>Yang B</pubmed_authors><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Li L</pubmed_authors><pubmed_authors>Bai X</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Ren H</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Gao W</pubmed_authors><pubmed_authors>Xu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Annexin A1 protects against cerebral ischemia-reperfusion injury by modulating microglia/macrophage polarization via FPR2/ALX-dependent AMPK-mTOR pathway.</name><description>&lt;h4>Background&lt;/h4>Cerebral ischemia-reperfusion (I/R) injury is a major cause of early complications and unfavorable outcomes after endovascular thrombectomy (EVT) therapy in patients with acute ischemic stroke (AIS). Recent studies indicate that modulating microglia/macrophage polarization and subsequent inflammatory response may be a potential adjunct therapy to recanalization. Annexin A1 (ANXA1) exerts potent anti-inflammatory and pro-resolving properties in models of cerebral I/R injury. However, whether ANXA1 modulates post-I/R-induced microglia/macrophage polarization has not yet been fully elucidated.&lt;h4>Methods&lt;/h4>We retrospectively collected blood samples from AIS patients who underwent successful recanalization by EVT and analyzed ANXA1 levels longitudinally before and after EV</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2025-04-04T20:17:53.305Z</modification><creation>2025-04-04T20:17:53.305Z</creation></dates><accession>S-EPMC8140477</accession><cross_references><pubmed>34022892</pubmed><doi>10.1186/s12974-021-02174-3</doi></cross_references></HashMap>