{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Subati T"],"funding":["BLRD VA","NHLBI NIH HHS"],"pagination":["e013199"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11919554"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(3)"],"pubmed_abstract":["<h4>Background</h4>The strongest genetic risk factors for atrial fibrillation (AF) are DNA variants on chromosome 4q25 near the transcription factor gene <i>PITX2</i> (Pitx2:Paired-like homeodomain transcription factor 2). Mice deficient in <i>Pitx2</i> (<i>Pitx2</i><sup><i>+/-</i></sup>) have increased AF susceptibility, although the molecular mechanism(s) remains controversial. <i>Pitx2</i> encodes a transcription factor that activates an antioxidant response to promote cardiac repair. Increased reactive oxygen species causing oxidation of polyunsaturated fatty acids generates reactive lipid dicarbonyl moieties that adduct to proteins and other macromolecules to promote cellular injury. We tested the hypothesis that oxidative stress, and specifically isolevuglandins, the most reactive li"],"journal":["Circulation. Arrhythmia and electrophysiology"],"pubmed_title":["Oxidative Stress Causes Mitochondrial and Electrophysiologic Dysfunction to Promote Atrial Fibrillation in &lt;i&gt;Pitx2&lt;sup&gt;+/-&lt;/sup&gt;&lt;/i&gt; Mice."],"pmcid":["PMC11919554"],"funding_grant_id":["R01 HL096844","IK2 BX005828"],"pubmed_authors":["Barnett JV","Dougherty OP","Saffitz JE","Agrawal V","Subati T","Kim K","Murphy MB","Christopher IL","Fogo AB","Van Amburg JC","Johnson JE","Woodall KK","Yang Z","Smart CD","Murray KT","Amarnath V"],"additional_accession":[]},"is_claimable":false,"name":"Oxidative Stress Causes Mitochondrial and Electrophysiologic Dysfunction to Promote Atrial Fibrillation in &lt;i&gt;Pitx2&lt;sup&gt;+/-&lt;/sup&gt;&lt;/i&gt; Mice.","description":"<h4>Background</h4>The strongest genetic risk factors for atrial fibrillation (AF) are DNA variants on chromosome 4q25 near the transcription factor gene <i>PITX2</i> (Pitx2:Paired-like homeodomain transcription factor 2). Mice deficient in <i>Pitx2</i> (<i>Pitx2</i><sup><i>+/-</i></sup>) have increased AF susceptibility, although the molecular mechanism(s) remains controversial. <i>Pitx2</i> encodes a transcription factor that activates an antioxidant response to promote cardiac repair. Increased reactive oxygen species causing oxidation of polyunsaturated fatty acids generates reactive lipid dicarbonyl moieties that adduct to proteins and other macromolecules to promote cellular injury. We tested the hypothesis that oxidative stress, and specifically isolevuglandins, the most reactive li","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-07-16T23:17:58.065Z","creation":"2026-07-12T03:11:27.002Z"},"accession":"S-EPMC11919554","cross_references":{"pubmed":["39989351"],"doi":["10.1161/CIRCEP.124.013199","10.1161/circep.124.013199"]}}