Targeting cardiomyocyte Ca2+ homeostasis in heart failure

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Updated: Apr 19, 2026

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.7K

Asmund T Roe, Michael Frisk, William E Louch1

  • 1Institute for Experimental Medical Research, Kirkeveien 166, 4.etg. Bygg 7, Oslo University Hospital Ullevål, 0407 Oslo, Norway. w.e.louch@medisin.uio.no.

Current Pharmaceutical Design
|December 9, 2014
PubMed

Insights

Disrupted calcium (Ca2+) handling in heart muscle cells contributes to heart failure. Targeting key proteins like the sarcoplasmic reticulum Ca2+ ATPase and Na+-Ca2+ exchanger offers promising therapeutic strategies.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Disrupted cardiomyocyte calcium (Ca2+) homeostasis is a critical factor in heart failure.
  • This disruption contributes to systolic/diastolic dysfunction, arrhythmias, and cell death signaling.

Purpose of the Study:

  • To review the role of Ca2+ homeostasis in heart failure.
  • To identify and discuss novel therapeutic targets for heart failure treatment.

Main Methods:

  • Literature review of existing knowledge on Ca2+ homeostasis in heart failure.
  • Analysis of experimental data for potential therapeutic targets.

Main Results:

  • Four key targets identified: sarcoplasmic reticulum Ca2+ ATPase, Na+-Ca2+ exchanger, ryanodine receptor, and t-tubule structure.
  • Experimental data supports the clinical applicability of these targets.

Conclusions:

  • Targeting Ca2+ handling mechanisms presents a promising avenue for improved heart failure treatments.
  • Ongoing clinical trials and future approaches are discussed based on these targets.

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