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Microcurrent stimulation promotes reverse remodelling in cardiomyocytes.

Barbara Kapeller1, Johannes Mueller2, Udo Losert1

  • 1Department for Biomedical Research Medical University Vienna Vienna Austria.

ESC Heart Failure
|October 25, 2016
PubMed
Summary
This summary is machine-generated.

Microcurrent (MC) stimulation modulated matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) in heart cells. This finding suggests potential new treatments for heart failure by targeting extracellular matrix remodeling.

Keywords:
CardiomyocytesExtracellular matrixMMP/TIMPMicrocurrent

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Area of Science:

  • Cardiovascular Research
  • Biomedical Engineering
  • Cell Biology

Background:

  • Heart failure is associated with imbalances in extracellular matrix composition.
  • Electrical stimulation shows promise for improving tissue repair.
  • Matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) play crucial roles in cardiac remodeling.

Purpose of the Study:

  • To investigate the effect of microcurrent (MC) on MMP and TIMP expression in cardiomyocytes.
  • To assess MC's potential to reverse cardiac remodeling in spontaneous hypertensive rats (SHR).

Main Methods:

  • Cardiomyocytes from young and old SHR were stimulated with MC in vitro and in vivo.
  • Gene and protein expression of MMPs and TIMPs were analyzed using qPCR and immunofluorescence.

Main Results:

  • MC stimulation enhanced cardiomyocyte proliferation in vitro without altering morphology.
  • MC exhibited dual effects on MMP-2, MMP-9, TIMP-3, and TIMP-4 expression, varying with cardiomyocyte age.
  • In vivo, MC down-regulated MMP-2, MMP-9, and TIMP-4 while up-regulating TIMP-3 in young SHR; old SHR showed upregulation of MMP-2, MMP-9, and TIMP-4, with unaffected TIMP-3.

Conclusions:

  • Microcurrent treatment can modulate MMP and TIMP expression in cardiomyocytes both in vitro and in vivo in SHR models.
  • These findings support the development of novel therapeutic strategies for heart failure targeting extracellular matrix modulation.