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Intracellular devastation in heart failure

Federica Del Monte1, Roger J Hajjar

  • 1Cardiovascular Research, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, USA. fdelmont@bidmc.harvard.edu

Heart Failure Reviews
|March 19, 2008
PubMed

Insights

End-stage heart failure involves cellular changes like impaired calcium cycling and protein misfolding. Targeting these abnormalities offers potential therapeutic strategies for cardiac dysfunction.

Area of Science:

  • Cardiology
  • Cellular Biology
  • Biochemistry

Background:

  • End-stage heart failure presents complex cellular abnormalities.
  • These include altered excitation-contraction coupling and signaling pathways.
  • While some changes are adaptive, many are detrimental to cardiac cells.

Purpose of the Study:

  • To review cellular calcium cycling changes in myopathic hearts.
  • To explore therapeutic targeting of these calcium cycling abnormalities.
  • To focus on the role of protein misfolding in cardiac dysfunction.

Main Methods:

  • Literature review of cellular mechanisms in heart failure.
  • Analysis of calcium cycling alterations in cardiac cells.
  • Examination of protein misfolding in myocardial disease.

Main Results:

  • Significant alterations in calcium cycling are observed in heart failure.
  • Protein misfolding contributes to cardiac dysfunction.
  • These cellular changes impact overall cardiac performance.

Conclusions:

  • Targeting aberrant calcium cycling presents a promising therapeutic avenue.
  • Addressing protein misfolding is crucial for managing cardiac dysfunction.
  • Understanding cellular changes is key to developing effective heart failure treatments.

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