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Measuring Fast Calcium Fluxes in Cardiomyocytes
12:10

Measuring Fast Calcium Fluxes in Cardiomyocytes

Published on: November 29, 2011

Calcium in the heart: when it's good, it's very very good, but when it's bad, it's horrid

H L Roderick1, D R Higazi, I Smyrnias

  • 1Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, U.K. Llewelyn.roderick@bbsrc.ac.uk

Biochemical Society Transactions
|October 25, 2007
PubMed

Insights

Calcium (Ca2+) signaling in the heart regulates contraction and growth. This review discusses how Ca2+ changes contribute to cardiac hypertrophy and failure, impacting heart function.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Biology
  • Molecular Cardiology

Background:

  • Cardiac function relies on intracellular calcium (Ca2+) transients.
  • Short-term increases in Ca2+ enhance heart contraction for increased demand.
  • Prolonged Ca2+ signaling can lead to cardiac hypertrophy.

Purpose of the Study:

  • To discuss the role of Ca2+ in inducing cardiac hypertrophy.
  • To examine the impact of cardiac hypertrophy and failure on Ca2+ fluxes.
  • To explore the relationship between Ca2+ signaling and heart function in health and disease.

Main Methods:

  • Literature review of studies on cardiac Ca2+ signaling.
  • Analysis of the mechanisms linking Ca2+ to myocyte contraction and transcription.
  • Examination of Ca2+ dysregulation in pathological cardiac remodeling.

Main Results:

  • Ca2+ increases are crucial for both short-term contractile responses and long-term cardiac growth.
  • In decompensated heart failure, Ca2+ signaling capacity and cardiac output are diminished.
  • Cardiac hypertrophy progression is associated with altered Ca2+ handling.

Conclusions:

  • Ca2+ plays a dual role in cardiac adaptation and maladaptation.
  • Understanding Ca2+ fluxes is critical for comprehending heart hypertrophy and failure.
  • Dysfunctional Ca2+ signaling is a key feature of advanced heart disease.

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