<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang Y</submitter><funding>NHLBI NIH HHS</funding><pagination>e007322</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6494091</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(5)</volume><pubmed_abstract>The ATP-sensitive K&lt;sup>+&lt;/sup> (K&lt;sub>ATP&lt;/sub>) channels are hetero-octameric protein complexes comprising 4 pore-forming (Kir6.x) subunits and 4 regulatory sulfonylurea receptor (SURx) subunits. They are prominent in myocytes, pancreatic β cells, and neurons and link cellular metabolism with membrane excitability. Using genetically modified animals and genomic analysis in patients, recent studies have implicated certain ATP-sensitive K&lt;sup>+&lt;/sup> channel subtypes in physiological and pathological processes in a variety of cardiovascular diseases. In this review, we focus on the causal relationship between ATP-sensitive K&lt;sup>+&lt;/sup> channel activity and pathophysiology in the cardiovascular system, particularly from the perspective of genetic changes in human and animal models.</pubmed_abstract><journal>Circulation. Arrhythmia and electrophysiology</journal><pubmed_title>Genetic Discovery of ATP-Sensitive K&lt;sup>+&lt;/sup> Channels in Cardiovascular Diseases.</pubmed_title><pmcid>PMC6494091</pmcid><funding_grant_id>R35 HL140024</funding_grant_id><funding_grant_id>R01 HL045742</funding_grant_id><pubmed_authors>Nichols CG</pubmed_authors><pubmed_authors>Huang C</pubmed_authors><pubmed_authors>Hu D</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic Discovery of ATP-Sensitive K&lt;sup>+&lt;/sup> Channels in Cardiovascular Diseases.</name><description>The ATP-sensitive K&lt;sup>+&lt;/sup> (K&lt;sub>ATP&lt;/sub>) channels are hetero-octameric protein complexes comprising 4 pore-forming (Kir6.x) subunits and 4 regulatory sulfonylurea receptor (SURx) subunits. They are prominent in myocytes, pancreatic β cells, and neurons and link cellular metabolism with membrane excitability. Using genetically modified animals and genomic analysis in patients, recent studies have implicated certain ATP-sensitive K&lt;sup>+&lt;/sup> channel subtypes in physiological and pathological processes in a variety of cardiovascular diseases. In this review, we focus on the causal relationship between ATP-sensitive K&lt;sup>+&lt;/sup> channel activity and pathophysiology in the cardiovascular system, particularly from the perspective of genetic changes in human and animal models.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 May</publication><modification>2024-02-15T09:44:00.144Z</modification><creation>2020-05-22T18:58:40Z</creation></dates><accession>S-EPMC6494091</accession><cross_references><pubmed>31030551</pubmed><doi>10.1161/CIRCEP.119.007322</doi><doi>10.1161/circep.119.007322</doi></cross_references></HashMap>