<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Garbincius JF</submitter><funding>NIA NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NINDS NIH HHS</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>Mitochondrial calcium (&lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup>) uptake through the mitochondrial calcium uniporter channel (mtCU) stimulates metabolism to meet acute increases in cardiac energy demand. However, excessive &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> uptake during stress, as in ischemia-reperfusion, initiates permeability transition and cell death. Despite these often-reported acute physiological and pathological effects, a major unresolved controversy is whether mtCU-dependent &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> uptake and long-term elevation of cardiomyocyte &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> contributes to the heart's adaptation during sustained increases in workload.&lt;h4>Objective&lt;/h4>We tested the hypothesis that mtCU-dependent &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> uptake contributes to cardiac adaptation</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.04.17.537222</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10153142</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MCU gain- and loss-of-function models define the duality of mitochondrial calcium uptake in heart failure.</pubmed_title><pmcid>PMC10153142</pmcid><funding_grant_id>P01 HL147841</funding_grant_id><funding_grant_id>R01 HL123966</funding_grant_id><funding_grant_id>F32 HL151146</funding_grant_id><funding_grant_id>T32 HL091804</funding_grant_id><funding_grant_id>R00 AG065445</funding_grant_id><funding_grant_id>R01 HL142271</funding_grant_id><funding_grant_id>P01 HL134608</funding_grant_id><funding_grant_id>R01 HL136954</funding_grant_id><funding_grant_id>RF1 NS121379</funding_grant_id><pubmed_authors>Garbincius JF</pubmed_authors><pubmed_authors>Elrod JW</pubmed_authors><pubmed_authors>Lambert JP</pubmed_authors><pubmed_authors>Mangold AS</pubmed_authors><pubmed_authors>Murray EK</pubmed_authors><pubmed_authors>Jadiya P</pubmed_authors><pubmed_authors>Luongo TS</pubmed_authors><pubmed_authors>Hildebrand AN</pubmed_authors></additional><is_claimable>false</is_claimable><name>MCU gain- and loss-of-function models define the duality of mitochondrial calcium uptake in heart failure.</name><description>&lt;h4>Background&lt;/h4>Mitochondrial calcium (&lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup>) uptake through the mitochondrial calcium uniporter channel (mtCU) stimulates metabolism to meet acute increases in cardiac energy demand. However, excessive &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> uptake during stress, as in ischemia-reperfusion, initiates permeability transition and cell death. Despite these often-reported acute physiological and pathological effects, a major unresolved controversy is whether mtCU-dependent &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> uptake and long-term elevation of cardiomyocyte &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> contributes to the heart's adaptation during sustained increases in workload.&lt;h4>Objective&lt;/h4>We tested the hypothesis that mtCU-dependent &lt;sub>m&lt;/sub>Ca&lt;sup>2+&lt;/sup> uptake contributes to cardiac adaptation</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-05-10T03:08:24.701Z</modification><creation>2025-04-05T21:09:17.432Z</creation></dates><accession>S-EPMC10153142</accession><cross_references><pubmed>37131819</pubmed><doi>10.1101/2023.04.17.537222</doi></cross_references></HashMap>