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CaMKII: do not work too hard in the failing heart

Min Liu1, You Li, Ruichuan Chen

  • 1State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, 361101, China.

The Journal of Pathology
|January 8, 2015
PubMed

Insights

Calcium/calmodulin-dependent protein kinase II delta (CaMKIIδ) is elevated in heart disease, driving pathological hypertrophy and heart failure by activating fetal genes. This suggests current heart failure therapies may pose risks.

Area of Science:

  • Cardiovascular Biology
  • Molecular Pathology
  • Gene Regulation

Background:

  • Calcium/calmodulin-dependent protein kinase II delta (CaMKIIδ) is implicated in cardiac pathophysiology.
  • Distinguishing between pathological hypertrophy and heart failure remains a clinical challenge.

Purpose of the Study:

  • To investigate the role of CaMKIIδ in pathological cardiac hypertrophy and heart failure.
  • To elucidate the molecular mechanisms by which CaMKIIδ influences cardiac gene expression.

Main Methods:

  • Analysis of CaMKIIδ levels in human and mouse heart samples.
  • Investigation of CaMKIIδ-mediated histone modification and protein interactions.
  • Assessment of CaMKIIδ's role in regulating fetal gene transcription.

Main Results:

  • CaMKIIδ levels are increased in both pathological cardiac hypertrophy and heart failure.
  • CaMKIIδ phosphorylates histone H3 at serine 10 (H3S10).
  • H3S10 phosphorylation recruits 14-3-3 proteins, activating fetal gene transcription.

Conclusions:

  • CaMKIIδ is a key mediator linking pathological hypertrophy to heart failure.
  • The findings suggest a continuum between these cardiac conditions.
  • Current heart failure treatments may carry risks due to CaMKIIδ involvement.

Keywords:
CaMKIIδheart failurepathological hypertrophy

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