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