The interplay of signaling pathway in endothelial cells-matrix stiffness dependency with targeted-therapeutic drugs

Vicki Vania1, Lu Wang1, Marco Tjakra1

  • 1Key Laboratory for Biorheological Science and Technology of Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, Bioengineering College of Chongqing University, Chongqing 400030, China.

Insights

Matrix stiffness significantly influences cardiovascular diseases (CVDs) by affecting endothelial cells. Understanding these mechanobiology pathways, like RhoA/ROCK and MAPK, is crucial for developing new CVD therapies.

Area of Science:

  • Mechanobiology
  • Cardiovascular Research
  • Cellular Pathophysiology

Background:

  • Cardiovascular diseases (CVDs) are a leading cause of global mortality.
  • Cell chemotaxis has been a long-standing focus in CVD research.
  • Mechanical stimuli increasingly recognized for their role in arterial pathophysiology and endothelial dysfunction, key to atherosclerosis.

Purpose of the Study:

  • To review how matrix stiffness mediates atherogenesis in endothelial cells.
  • To explore signaling pathways (RhoA/ROCK, MAPK, Hippo) and mechanosensitive non-coding RNAs involved.
  • To discuss tunable hydrogels for advancing CVD research.

Main Methods:

  • Literature review focusing on mechanobiology and CVD.
  • Analysis of signaling pathways influenced by matrix stiffness.
  • Examination of non-coding RNAs in matrix stiffness-mediated atherogenesis.

Main Results:

  • Matrix stiffness impacts endothelial cells through RhoA/ROCK, MAPK, and Hippo pathways.
  • Mechanosensitive non-coding RNAs play a role in matrix stiffness-driven atherogenesis.
  • Tunable hydrogels offer potential for future research strategies.

Conclusions:

  • Matrix stiffness is a critical factor in cardiovascular disease development.
  • Targeting mechanobiology pathways presents therapeutic opportunities for CVDs.
  • Further research using advanced materials like tunable hydrogels is needed.

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