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3D matrix stiffness modulation unveils cardiac fibroblast phenotypic switching
Yan Han1, Zehua Shao2, Yuanhao Zhang1
1Department of Structural Heart Disease, Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, 451464, Henan, China.
Scientific Reports
|July 23, 2024
Summary
Matrix stiffness influences cardiac fibroblast behavior. Increased stiffness promotes myofibroblast differentiation, while softening reverses it, offering potential therapeutic strategies for cardiovascular diseases.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Cardiovascular Research
Background:
- Cardiac fibroblasts (CFs) play a key role in cardiac fibrosis.
- The cardiac microenvironment exhibits dynamic stiffness changes.
- Understanding CF mechanobiology is crucial for treating heart disease.
Purpose of the Study:
- To investigate the impact of dynamic matrix stiffness on CF behavior.
- To explore the role of stiffness in myofibroblast differentiation.
- To identify mechanotransduction pathways involved in CF responses.
Main Methods:
- Utilized 3D hybrid hydrogels with tunable stiffness to mimic cardiac microenvironment.
- Quantified CF differentiation by measuring α-smooth muscle actin (α-SMA) expression.
- Assessed the involvement of focal adhesions and integrin β1.
Main Results:
- Increased matrix stiffness significantly promoted CF differentiation into myofibroblasts.
- Matrix softening reversed myofibroblast differentiation.
- Focal adhesions and integrin β1 were identified as key mediators of stiffness-induced phenotypic switching.
Conclusions:
- Dynamic matrix stiffness is a critical regulator of cardiac fibroblast phenotype.
- Modulating matrix stiffness may represent a novel therapeutic approach for cardiac fibrosis.
- This study advances the understanding of cardiac mechanobiology and fibrosis.
