<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang Y</submitter><funding>Key Technologies Research and Development Program</funding><funding>Natural Science Foundation of Tianjin Municipality</funding><funding>National Natural Science Foundation of China</funding><pagination>264</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11335301</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>81(1)</volume><pubmed_abstract>Atrial fibrillation (AF) is the most common arrhythmia, and atrial fibrosis is a pathological hallmark of structural remodeling in AF. Prostaglandin I&lt;sub>2&lt;/sub> (PGI&lt;sub>2&lt;/sub>) can prevent the process of fibrosis in various tissues via cell surface Prostaglandin I&lt;sub>2&lt;/sub> receptor (IP). However, the role of PGI&lt;sub>2&lt;/sub> in AF and atrial fibrosis remains unclear. The present study aimed to clarify the role of PGI&lt;sub>2&lt;/sub> in angiotensin II (Ang II)-induced AF and the underlying molecular mechanism. PGI&lt;sub>2&lt;/sub> content was decreased in both plasma and atrial tissue from patients with AF and mice treated with Ang II. Treatment with the PGI&lt;sub>2&lt;/sub> analog, iloprost, reduced Ang II-induced AF and atrial fibrosis. Iloprost prevented Ang II-induced atrial fibroblast collagen</pubmed_abstract><journal>Cellular and molecular life sciences : CMLS</journal><pubmed_title>Prostaglandin I&lt;sub>2&lt;/sub> signaling prevents angiotensin II-induced atrial remodeling and vulnerability to atrial fibrillation in mice.</pubmed_title><pmcid>PMC11335301</pmcid><funding_grant_id>18JCQNJC82600</funding_grant_id><funding_grant_id>82000272</funding_grant_id><funding_grant_id>81800297</funding_grant_id><funding_grant_id>2020YFA0803703</funding_grant_id><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Yuan M</pubmed_authors><pubmed_authors>Sun W</pubmed_authors><pubmed_authors>Yan Y</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Shi X</pubmed_authors><pubmed_authors>Bao Q</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Liu D</pubmed_authors><pubmed_authors>Song W</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Cai W</pubmed_authors><pubmed_authors>Chen T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prostaglandin I&lt;sub>2&lt;/sub> signaling prevents angiotensin II-induced atrial remodeling and vulnerability to atrial fibrillation in mice.</name><description>Atrial fibrillation (AF) is the most common arrhythmia, and atrial fibrosis is a pathological hallmark of structural remodeling in AF. Prostaglandin I&lt;sub>2&lt;/sub> (PGI&lt;sub>2&lt;/sub>) can prevent the process of fibrosis in various tissues via cell surface Prostaglandin I&lt;sub>2&lt;/sub> receptor (IP). However, the role of PGI&lt;sub>2&lt;/sub> in AF and atrial fibrosis remains unclear. The present study aimed to clarify the role of PGI&lt;sub>2&lt;/sub> in angiotensin II (Ang II)-induced AF and the underlying molecular mechanism. PGI&lt;sub>2&lt;/sub> content was decreased in both plasma and atrial tissue from patients with AF and mice treated with Ang II. Treatment with the PGI&lt;sub>2&lt;/sub> analog, iloprost, reduced Ang II-induced AF and atrial fibrosis. Iloprost prevented Ang II-induced atrial fibroblast collagen</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jun</publication><modification>2025-04-26T21:22:55.014Z</modification><creation>2025-04-06T16:45:19.249Z</creation></dates><accession>S-EPMC11335301</accession><cross_references><pubmed>38878214</pubmed><doi>10.1007/s00018-024-05259-3</doi></cross_references></HashMap>