Mitochondrial Ca2+ uptake: Tortoise or hare?

Brian O'Rourke, Lothar A. Blatter

Research output: Contribution to journalComment/debatepeer-review

73 Scopus citations


Mitochondria are equipped with an efficient machinery for Ca2+ uptake and extrusion and are capable of storing large amounts of Ca2+. Furthermore, key steps of mitochondrial metabolism (ATP production) are Ca2+-dependent. In the field of cardiac physiology and pathophysiology, two main questions have dominated the thinking about mitochondrial function in the heart: 1) how does mitochondrial Ca2+ buffering shape cytosolic Ca2+ levels and affect excitation-contraction coupling, particularly the Ca2+ transient, on a beat-to-beat basis, and 2) how does mitochondrial Ca2+ homeostasis influence cardiac energy metabolism. To answer these questions, a thorough understanding of the kinetics of mitochondrial Ca2+ transport and buffer capacity is required. Here, we summarize the role of mitochondrial Ca2+ signaling in the heart, discuss the evidence either supporting or arguing against the idea that Ca2+ can be taken up rapidly by mitochondria during excitation-contraction coupling and highlight some interesting new areas for further investigation.

Original languageEnglish (US)
Pages (from-to)767-774
Number of pages8
JournalJournal of Molecular and Cellular Cardiology
Issue number6
StatePublished - Jun 2009


  • Ca transients
  • Calcium uniporter
  • Cellular energetics
  • Energy metabolism
  • Excitation-contraction coupling
  • Mitochondrial inner membrane
  • Sodium-calcium exchange

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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