Role of mitochondrial Ca 2+ homeostasis in cardiac muscles

Jessica L. Cao, Stephanie M. Adaniya, Michael W. Cypress, Yuta Suzuki, Yoichiro Kusakari, Bong Sook Jhun, Jin O-Uchi

Research output: Contribution to journalReview articlepeer-review

7 Scopus citations

Abstract

Recent discoveries of the molecular identity of mitochondrial Ca 2+ influx/efflux mechanisms have placed mitochondrial Ca 2+ transport at center stage in views of cellular regulation in various cell-types/tissues. Indeed, mitochondria in cardiac muscles also possess the molecular components for efficient uptake and extraction of Ca 2+ . Over the last several years, multiple groups have taken advantage of newly available molecular information about these proteins and applied genetic tools to delineate the precise mechanisms for mitochondrial Ca 2+ handling in cardiomyocytes and its contribution to excitation-contraction/metabolism coupling in the heart. Though mitochondrial Ca 2+ has been proposed as one of the most crucial secondary messengers in controlling a cardiomyocyte's life and death, the detailed mechanisms of how mitochondrial Ca 2+ regulates physiological mitochondrial and cellular functions in cardiac muscles, and how disorders of this mechanism lead to cardiac diseases remain unclear. In this review, we summarize the current controversies and discrepancies regarding cardiac mitochondrial Ca 2+ signaling that remain in the field to provide a platform for future discussions and experiments to help close this gap.

Original languageEnglish (US)
Pages (from-to)276-287
Number of pages12
JournalArchives of Biochemistry and Biophysics
Volume663
DOIs
StatePublished - Mar 15 2019

Bibliographical note

Funding Information:
J.L.C. and S.M.A. were supported by the Brown University Karen T. Romer Undergraduate Teaching and Research Awards (UTRA). B.S.J was supported by NIH/NIGMS U54GM115677 and American Heart Association 18CDA34110091 . J.O.-U. was supported by NIH/NHLBI R01HL136757 , NIH/NIGMS P30GM1114750 , AHA 16SDG27260248 , Rhode Island Foundation No. 20164376 Medical Research Grant, American Physiological Society (APS) 2017 Shih-Chun Wang Young Investigator Award.

Funding Information:
J.L.C. and S.M.A. were supported by the Brown University Karen T. Romer Undergraduate Teaching and Research Awards (UTRA). B.S.J was supported by NIH/NIGMS U54GM115677 and American Heart Association 18CDA34110091. J.O.-U. was supported by NIH/NHLBI R01HL136757, NIH/NIGMS P30GM1114750, AHA 16SDG27260248, Rhode Island Foundation No. 20164376 Medical Research Grant, American Physiological Society (APS) 2017 Shih-Chun Wang Young Investigator Award.

Publisher Copyright:
© 2019 Elsevier Inc.

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