Mitochondrial Ca2+ in heart failure: Not enough or too much?

Brian O'Rourke, Deepthi Ashok, Ting Liu

Research output: Contribution to journalArticlepeer-review

Abstract

Ca2+ serves as a ubiquitous second messenger mediating a variety of cellular processes including electrical excitation, contraction, gene expression, secretion, cell death and others. The identification of the molecular components of the mitochondrial Ca2+ influx and efflux pathways has created a resurgent interest in the regulation of mitochondrial Ca2+ balance and its physiological and pathophysiological roles. While the pace of discovery has quickened with the availability of new cellular and animal models, many fundamental questions remain to be answered regarding the regulation and functional impact of mitochondrial Ca2+ in health and disease. This review highlights several experimental observations pertaining to key aspects of mitochondrial Ca2+ homeostasis that remain enigmatic, particularly whether mitochondrial Ca2+ signaling is depressed or excessive in heart failure, which will determine the optimal approach to therapeutic intervention.

Original languageEnglish (US)
Pages (from-to)126-134
Number of pages9
JournalJournal of Molecular and Cellular Cardiology
Volume151
DOIs
StatePublished - Feb 2021

Keywords

  • Animal model
  • Heart failure
  • MCU
  • NCLX
  • ROS
  • Sudden cardiac death

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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