<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu H</submitter><funding>Educational Department of Liaoning Province</funding><funding>National Natural Science Foundation of China</funding><funding>Natural Science Foundation of Liaoning Province</funding><funding>Department of Science and Technology of Liaoning Province</funding><pagination>e202103098</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10067974</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>222(5)</volume><pubmed_abstract>Microvascular basement membrane (BM) plays a pivotal role in the interactions of astrocyte with endothelium to maintain the blood-brain barrier (BBB) homeostasis; however, the significance and precise regulation of the endothelial cell-derived BM component in the BBB remain incompletely understood. Here, we report that conditional knockout of Atg7 in endothelial cells (Atg7-ECKO) leads to astrocyte-microvascular disassociation in the brain. Our results reveal astrocytic endfeet detachment from microvessels and BBB leakage in Atg7-ECKO mice. Furthermore, we find that the absence of endothelial Atg7 downregulates the expression of fibronectin, a major BM component of the BBB, causing significantly reduced coverage of astrocytes along cerebral microvessels. We reveal Atg7 triggers the express</pubmed_abstract><journal>The Journal of cell biology</journal><pubmed_title>Endothelial depletion of Atg7 triggers astrocyte-microvascular disassociation at blood-brain barrier.</pubmed_title><pmcid>PMC10067974</pmcid><funding_grant_id>32171108</funding_grant_id><funding_grant_id>31171291</funding_grant_id><funding_grant_id>LT2016004</funding_grant_id><funding_grant_id>20170520420</funding_grant_id><funding_grant_id>31771258</funding_grant_id><funding_grant_id>2019JH2/10300020</funding_grant_id><funding_grant_id>31701024</funding_grant_id><funding_grant_id>31571057</funding_grant_id><funding_grant_id>31870832</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Cao L</pubmed_authors><pubmed_authors>Wei JY</pubmed_authors><pubmed_authors>Zhao WD</pubmed_authors><pubmed_authors>Yue JL</pubmed_authors><pubmed_authors>Shang DS</pubmed_authors><pubmed_authors>Jin YP</pubmed_authors><pubmed_authors>Fang WG</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Zhang HY</pubmed_authors><pubmed_authors>Tong PG</pubmed_authors><pubmed_authors>Liu DX</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Ban M</pubmed_authors><pubmed_authors>Sun Q</pubmed_authors><pubmed_authors>Chen YH</pubmed_authors><pubmed_authors>Zhao D</pubmed_authors><pubmed_authors>Li B</pubmed_authors><pubmed_authors>Wang KJ</pubmed_authors><pubmed_authors>Wang HJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Endothelial depletion of Atg7 triggers astrocyte-microvascular disassociation at blood-brain barrier.</name><description>Microvascular basement membrane (BM) plays a pivotal role in the interactions of astrocyte with endothelium to maintain the blood-brain barrier (BBB) homeostasis; however, the significance and precise regulation of the endothelial cell-derived BM component in the BBB remain incompletely understood. Here, we report that conditional knockout of Atg7 in endothelial cells (Atg7-ECKO) leads to astrocyte-microvascular disassociation in the brain. Our results reveal astrocytic endfeet detachment from microvessels and BBB leakage in Atg7-ECKO mice. Furthermore, we find that the absence of endothelial Atg7 downregulates the expression of fibronectin, a major BM component of the BBB, causing significantly reduced coverage of astrocytes along cerebral microvessels. We reveal Atg7 triggers the express</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 May</publication><modification>2026-05-29T08:04:18.452Z</modification><creation>2025-04-05T15:23:25.742Z</creation></dates><accession>S-EPMC10067974</accession><cross_references><pubmed>36995368</pubmed><doi>10.1083/jcb.202103098</doi></cross_references></HashMap>