<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zaglia T</submitter><funding>Telethon</funding><funding>European Research Council</funding><pagination>E9006-E9015</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5664523</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>114(43)</volume><pubmed_abstract>The mitochondrial Ca&lt;sup>2+&lt;/sup> uniporter complex (MCUC) is a multimeric ion channel which, by tuning Ca&lt;sup>2+&lt;/sup> influx into the mitochondrial matrix, finely regulates metabolic energy production. In the heart, this dynamic control of mitochondrial Ca&lt;sup>2+&lt;/sup> uptake is fundamental for cardiomyocytes to adapt to either physiologic or pathologic stresses. Mitochondrial calcium uniporter (MCU), which is the core channel subunit of MCUC, has been shown to play a critical role in the response to β-adrenoreceptor stimulation occurring during acute exercise. The molecular mechanisms underlying the regulation of MCU, in conditions requiring chronic increase in energy production, such as physiologic or pathologic cardiac growth, remain elusive. Here, we show that microRNA-1 (miR-1), a m</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy.</pubmed_title><pmcid>PMC5664523</pmcid><funding_grant_id>294777</funding_grant_id><funding_grant_id>GGP11224</funding_grant_id><pubmed_authors>Ulrik W</pubmed_authors><pubmed_authors>Cerbai E</pubmed_authors><pubmed_authors>Faggian G</pubmed_authors><pubmed_authors>De Stefani D</pubmed_authors><pubmed_authors>Sandri M</pubmed_authors><pubmed_authors>Pozzan T</pubmed_authors><pubmed_authors>Borile G</pubmed_authors><pubmed_authors>Ceriotti P</pubmed_authors><pubmed_authors>Stellin G</pubmed_authors><pubmed_authors>Stolen TO</pubmed_authors><pubmed_authors>Vida V</pubmed_authors><pubmed_authors>Di Lisa F</pubmed_authors><pubmed_authors>Campo A</pubmed_authors><pubmed_authors>Carullo P</pubmed_authors><pubmed_authors>Zaglia T</pubmed_authors><pubmed_authors>Coppini R</pubmed_authors><pubmed_authors>Catalucci D</pubmed_authors><pubmed_authors>Prando V</pubmed_authors><pubmed_authors>Mongillo M</pubmed_authors><pubmed_authors>Armani A</pubmed_authors><pubmed_authors>Rizzuto R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy.</name><description>The mitochondrial Ca&lt;sup>2+&lt;/sup> uniporter complex (MCUC) is a multimeric ion channel which, by tuning Ca&lt;sup>2+&lt;/sup> influx into the mitochondrial matrix, finely regulates metabolic energy production. In the heart, this dynamic control of mitochondrial Ca&lt;sup>2+&lt;/sup> uptake is fundamental for cardiomyocytes to adapt to either physiologic or pathologic stresses. Mitochondrial calcium uniporter (MCU), which is the core channel subunit of MCUC, has been shown to play a critical role in the response to β-adrenoreceptor stimulation occurring during acute exercise. The molecular mechanisms underlying the regulation of MCU, in conditions requiring chronic increase in energy production, such as physiologic or pathologic cardiac growth, remain elusive. Here, we show that microRNA-1 (miR-1), a m</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Oct</publication><modification>2025-04-04T14:10:23.775Z</modification><creation>2019-06-06T18:21:45Z</creation></dates><accession>S-EPMC5664523</accession><cross_references><pubmed>29073097</pubmed><doi>10.1073/pnas.1708772114</doi></cross_references></HashMap>