<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zou Z</submitter><funding>Research Cooperation Platform Project of Sino-Japanese Friendship Hospital of Jilin University and Basic Medical School of Jilin University</funding><funding>National Natural Science Foundation of China</funding><funding>Department of Science and Technology of Jilin Province</funding><pagination>e70615</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12445200</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(9)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Ferroptosis is an essential pathophysiological process in cerebral ischemic injury. Activin receptor-interacting protein 1 (ARIP1) is a negative regulator of the activin signaling pathway in neurons.&lt;h4>Objective&lt;/h4>This study investigated whether activin A inhibits neuronal ferroptosis and the role of ARIP1 in cerebral ischemic injury.&lt;h4>Methods and results&lt;/h4>In this study, activin A increased the viability of primary neurons under conditions of oxygen-glucose deprivation (OGD). Subsequent RNA-sequencing analysis of activin A-treated neurons identified expression of Slc7a11 as the ferroptosis-associated gene with significant upregulation. Next, using the CRISPR/Cas9 system, mice were generated with a heterozygous deficiency of ARIP1 (Arip1&lt;sup>-/+&lt;/sup>), and the </pubmed_abstract><journal>CNS neuroscience &amp; therapeutics</journal><pubmed_title>ARIP1 Deficiency Facilitates the Inhibition of Neuronal Ferroptosis in Cerebral Ischemia by Activin A Through SMAD3 and p38 MAPK Signaling.</pubmed_title><pmcid>PMC12445200</pmcid><funding_grant_id>81971174</funding_grant_id><funding_grant_id>20230505042ZP</funding_grant_id><funding_grant_id>81371445</funding_grant_id><funding_grant_id>KYXZ2022JC04</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Xie D</pubmed_authors><pubmed_authors>Zou Z</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Qie X</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Guo C</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>ARIP1 Deficiency Facilitates the Inhibition of Neuronal Ferroptosis in Cerebral Ischemia by Activin A Through SMAD3 and p38 MAPK Signaling.</name><description>&lt;h4>Introduction&lt;/h4>Ferroptosis is an essential pathophysiological process in cerebral ischemic injury. Activin receptor-interacting protein 1 (ARIP1) is a negative regulator of the activin signaling pathway in neurons.&lt;h4>Objective&lt;/h4>This study investigated whether activin A inhibits neuronal ferroptosis and the role of ARIP1 in cerebral ischemic injury.&lt;h4>Methods and results&lt;/h4>In this study, activin A increased the viability of primary neurons under conditions of oxygen-glucose deprivation (OGD). Subsequent RNA-sequencing analysis of activin A-treated neurons identified expression of Slc7a11 as the ferroptosis-associated gene with significant upregulation. Next, using the CRISPR/Cas9 system, mice were generated with a heterozygous deficiency of ARIP1 (Arip1&lt;sup>-/+&lt;/sup>), and the </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-03T15:14:52.078Z</modification><creation>2026-04-29T03:09:00.845Z</creation></dates><accession>S-EPMC12445200</accession><cross_references><pubmed>40965963</pubmed><doi>10.1111/cns.70615</doi></cross_references></HashMap>