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Cardiac Fibrotic Remodeling on a Chip with Dynamic Mechanical Stimulation.

Ming Kong1,2,3, Junmin Lee2,3,4,5,6,7, Iman K Yazdi2,3,4

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Mechanical compression regulates cardiac fibroblast (CFs) to myofibroblast transition in fibrosis. This study developed a microdevice to investigate strain-mediated cardiac remodeling, offering insights for new therapeutic strategies.

Keywords:
cardiac fibrosishydrogelsmechanical stimulationorgan-on-a-chiptransforming growth factor-β

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Area of Science:

  • Biomedical Engineering
  • Cardiovascular Research
  • Cell Biology

Background:

  • Cardiac tissue dynamics are crucial for physiological activity and pathological remodeling.
  • Fibrosis involves extracellular matrix remodeling and cardiac fibroblast (CFs) to myofibroblast transition.
  • Mechanical tension's role in regulating cardiac phenotypic transition during fibrosis is hypothesized.

Purpose of the Study:

  • To develop a microdevice mimicking cardiac biomechanical environments.
  • To investigate the strain-mediated regulation of cardiac fibroblast phenotypic transition.
  • To explore correlations between mechanical compression and fibrotic remodeling.

Main Methods:

  • A microdevice applying cyclic compressions (5-20% strain) to CF-laden GelMA hydrogels.
  • Tunable frequency and cytokine integration capabilities.
  • Investigation of CFs spreading, proliferation, and fibrotic phenotype remolding under varying mechanical loads.

Main Results:

  • Mechanical compression significantly influences CFs' phenotypic transition.
  • The effect of mechanical load is dependent on strain magnitude and myofibroblast maturity.
  • Evidence of a strain-response correlation in CFs' mechanical stimulation and remodeling.

Conclusions:

  • Mechanical stimulation, specifically strain, is a critical regulator of cardiac fibroblast phenotype.
  • Findings support the strain-mediated manner of cardiac phenotypic transition in fibrosis.
  • Results pave the way for novel preventive or therapeutic strategies for cardiac fibrosis.