Cadherin-11 and cardiac fibrosis: A common target for a common pathology

Lance A Riley1, W David Merryman1

  • 1Department of Biomedical Engineering, Vanderbilt University, USA.

Cellular Signalling
|December 7, 2020
PubMed

Insights

Cardiac fibrosis, a major heart disease complication, involves fibroblast activation, inflammation, and mechanical changes. Targeting cadherin-11 may offer new therapeutic strategies for heart disease.

Area of Science:

  • Cardiology
  • Cell Biology
  • Biomedical Engineering

Background:

  • Cardiac fibrosis is a key factor in cardiovascular diseases, the leading global cause of death.
  • Fibrosis involves fibroblast activation into myofibroblasts, excessive extracellular matrix deposition, persistent inflammation, and cellular responses to mechanical stress.

Purpose of the Study:

  • To review the mechanisms driving cardiac fibrosis in cardiovascular diseases.
  • To explore cadherin-11 as a potential therapeutic target linking fibrotic, inflammatory, and biomechanical pathways.

Main Methods:

  • Literature review of pro-fibrotic, pro-inflammatory, and biomechanical mechanisms in cardiac fibrosis.
  • Analysis of cadherin-11's role as an intercellular adhesion protein in myofibroblasts and inflammatory cells.

Main Results:

  • Cardiac fibrosis results from complex interactions between pro-fibrotic, pro-inflammatory, and biomechanical factors.
  • Cadherin-11 is identified as a potential unifying factor in these fibrotic mechanisms.
  • Blocking cadherin-11 dimerization has shown promise in preventing fibrotic diseases, including cardiac fibrosis.

Conclusions:

  • Understanding cadherin-11's role is crucial for developing novel therapeutic interventions for cardiac fibrosis.
  • Targeting cadherin-11 offers a potential strategy to treat cardiovascular diseases characterized by fibrosis.

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