<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Le Ribeuz H</submitter><pubmed_abstract>&lt;h4>Aims&lt;/h4>We hypothesized that the ATP-sensitive K&lt;sup>+&lt;/sup> channels (KATP) regulatory subunit (ABCC9) contributes to PAH pathogenesis. &lt;i>ABCC9&lt;/i> gene encodes for two regulatory subunits of KATP channels: the SUR2A and SUR2B proteins. In the KATP channel, the SUR2 subunits are associated with the K&lt;sup>+&lt;/sup> channel Kir6.1. We investigated how the SUR2/Kir6.1 channel contributes to PAH pathogenesis and its potential as a therapeutic target in PAH.&lt;h4>Methods and results&lt;/h4>Using &lt;i>in vitro, ex vivo&lt;/i>, and &lt;i>in vivo&lt;/i> approaches, we analyzed the localization and expression of SUR2A, SUR2B, and Kir6.1 in the pulmonary vasculature of controls and patients with PAH as in experimental pulmonary hypertension (PH) rat models and its contribution to PAH physiopathology. Finally, </pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>1066047</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9871631</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Involvement of SUR2/Kir6.1 channel in the physiopathology of pulmonary arterial hypertension.</pubmed_title><pmcid>PMC9871631</pmcid><pubmed_authors>Le Ribeuz H</pubmed_authors><pubmed_authors>Dutheil M</pubmed_authors><pubmed_authors>Beauvais A</pubmed_authors><pubmed_authors>Capuano V</pubmed_authors><pubmed_authors>Sabourin J</pubmed_authors><pubmed_authors>De Montpreville VT</pubmed_authors><pubmed_authors>Mercier O</pubmed_authors><pubmed_authors>Boet A</pubmed_authors><pubmed_authors>Antigny F</pubmed_authors><pubmed_authors>Masson B</pubmed_authors><pubmed_authors>Montani D</pubmed_authors><pubmed_authors>Humbert M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Involvement of SUR2/Kir6.1 channel in the physiopathology of pulmonary arterial hypertension.</name><description>&lt;h4>Aims&lt;/h4>We hypothesized that the ATP-sensitive K&lt;sup>+&lt;/sup> channels (KATP) regulatory subunit (ABCC9) contributes to PAH pathogenesis. &lt;i>ABCC9&lt;/i> gene encodes for two regulatory subunits of KATP channels: the SUR2A and SUR2B proteins. In the KATP channel, the SUR2 subunits are associated with the K&lt;sup>+&lt;/sup> channel Kir6.1. We investigated how the SUR2/Kir6.1 channel contributes to PAH pathogenesis and its potential as a therapeutic target in PAH.&lt;h4>Methods and results&lt;/h4>Using &lt;i>in vitro, ex vivo&lt;/i>, and &lt;i>in vivo&lt;/i> approaches, we analyzed the localization and expression of SUR2A, SUR2B, and Kir6.1 in the pulmonary vasculature of controls and patients with PAH as in experimental pulmonary hypertension (PH) rat models and its contribution to PAH physiopathology. Finally, </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-03-27T15:45:07.693Z</modification><creation>2025-04-05T21:41:09.311Z</creation></dates><accession>S-EPMC9871631</accession><cross_references><pubmed>36704469</pubmed><doi>10.3389/fcvm.2022.1066047</doi></cross_references></HashMap>