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Calcium signalling remodelling and disease

Michael J Berridge1

  • 1Babraham Institute, Babraham, Cambridge CB22 3AT, U.K. michael.berridge@babraham.ac.uk

Biochemical Society Transactions
|March 23, 2012
PubMed

Insights

Calcium (Ca2+) signaling is vital for cell function. Dysregulation of these signals, particularly through inositol 1,4,5-trisphosphate (InsP3) pathways, is linked to major human diseases like Alzheimer's and cardiac conditions.

Area of Science:

  • Cellular biology
  • Neuroscience
  • Biochemistry

Background:

  • Calcium (Ca2+) signaling pathways are crucial for diverse cellular functions.
  • Inositol 1,4,5-trisphosphate (InsP3)-mediated Ca2+ release is a key component of many signaling systems.
  • Transcriptional regulation maintains the stability of cell-specific Ca2+ signaling.

Purpose of the Study:

  • To explore the plasticity and dysregulation of Ca2+ signaling systems.
  • To investigate the link between altered Ca2+ signaling and human diseases.

Main Methods:

  • Analysis of Ca2+ signaling dynamics.
  • Investigation of transcriptional control mechanisms.
  • Review of disease-associated signaling alterations.

Main Results:

  • Ca2+ signaling systems exhibit phenotypic plasticity, allowing for remodeling.
  • Dysregulation, characterized by excessively high or low Ca2+ signals, can occur.
  • Subtle alterations in Ca2+ signaling are associated with major diseases, including cardiac disease, schizophrenia, bipolar disorder, and Alzheimer's disease.

Conclusions:

  • Cellular Ca2+ signaling is dynamic and susceptible to homeostatic imbalances.
  • Aberrant Ca2+ signaling represents a significant factor in the pathophysiology of various complex human diseases.
  • Understanding these signaling dysregulations may offer therapeutic targets for neurological and cardiac conditions.

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