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