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The calcium ion and cell death

S Orrenius1, P Nicotera

  • 1Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Journal of Neural Transmission. Supplementum
|January 1, 1994
PubMed
Summary

Calcium ion overload is critical in cell death, particularly in the central nervous system. Preventing this overload through various treatments can protect cells, highlighting its importance for neuroprotection strategies.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • The calcium ion (Ca2+) is a vital intracellular regulator of numerous physiological processes.
  • Disruption of intracellular Ca2+ homeostasis is linked to cell injury and cytotoxicity.
  • The calcium hypothesis of cell injury posits that perturbed Ca2+ homeostasis is a common step in cytotoxicity.

Purpose of the Study:

  • To review the critical role of calcium ions in cell killing, especially in the central nervous system.
  • To explore the biochemical mechanisms underlying Ca2+ overload-induced cell death (necrosis and apoptosis).
  • To discuss strategies for preventing Ca2+ overload for therapeutic benefit, particularly in neuroprotection.

Main Methods:

  • Review of existing research on calcium ion's role in cell death.
  • Analysis of biochemical pathways involved in intracellular Ca2+ overload.
  • Examination of studies demonstrating cell rescue by preventing Ca2+ overload.

Main Results:

  • Convincing evidence shows Ca2+ overload triggers necrotic or apoptotic cell death.
  • Pretreatment with Ca2+ chelators, receptor antagonists, or channel blockers can prevent cell death.
  • Cells expressing high levels of Ca(2+)-binding proteins exhibit increased resistance to killing.

Conclusions:

  • Preventing Ca2+ overload is crucial for mitigating cell death in various tissues, including the central nervous system.
  • Developing effective strategies to manage Ca2+ overload is essential for neuroprotection.
  • Understanding Ca2+ homeostasis is key to addressing cytotoxic processes.

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