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The ups and downs of mitochondrial calcium signalling in the heart

Elinor J Griffiths1, Dirki Balaska, Wendy H Y Cheng

  • 1Department of Biochemistry and Bristol Heart Institute, University of Bristol, School of Medical Sciences, University Walk, Bristol BS8 1TD, UK. Elinor.Griffiths@bristol.ac.uk

Biochimica Et Biophysica Acta
|March 2, 2010
PubMed

Insights

Mitochondrial calcium ([Ca2+]m) regulation is vital for heart function and disease. Ongoing research clarifies its roles in ATP production, cell signaling, and cell death, despite existing controversies.

Area of Science:

  • Cardiovascular Physiology
  • Mitochondrial Biology
  • Cellular Signaling

Background:

  • Intramitochondrial free calcium ([Ca2+]m) regulation is crucial for cardiac physiological and pathological processes.
  • Despite significant research, controversies persist regarding beat-to-beat mitochondrial calcium transients and their role in whole-cell calcium signaling.
  • The involvement of [Ca2+]m in coupling ATP supply and demand, and its role in necrosis and apoptosis, particularly in mitochondrial permeability transition pore formation, remain debated.

Purpose of the Study:

  • To summarize the key physiological roles of [Ca2+]m in ATP production and cell Ca2+ signaling in adult and neonatal hearts.
  • To highlight current controversies and recent advancements in understanding [Ca2+]m regulation in the heart.
  • To briefly discuss the interactions of nitric oxide with [Ca2+]m.

Main Methods:

  • Utilized advancements in fluorescent indicators, targeted proteins, and sensitive imaging technology for specific measurement of [Ca2+]m in intact cells and hearts.
  • Investigated interactions between mitochondrial calcium transporters (mCU, mNCX) and those of the sarcolemma and sarcoplasmic reticulum.
  • Reviewed existing literature to summarize physiological roles and controversies surrounding [Ca2+]m.

Main Results:

  • Developments in measurement techniques have revealed intricate interactions of mitochondrial calcium transporters with other cellular calcium handling systems.
  • Mitochondrial calcium uptake occurs via the ruthenium red-sensitive calcium uniporter (mCU), and efflux via the Na+/Ca2+ exchanger (mNCX).
  • Recent research highlights the role of [Ca2+]m in heart failure and its potential involvement in cell death pathways.

Conclusions:

  • Precise measurement of [Ca2+]m has advanced our understanding of its critical, yet elusive, role in cardiac function.
  • Further research, including transporter purification, cloning, and inhibitor development, is needed to resolve controversies and fully elucidate [Ca2+]m functions.
  • Understanding [Ca2+]m regulation is paramount for addressing cardiac pathologies and improving therapeutic strategies.

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