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Updated: Nov 17, 2025

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
Complex Relationship Between Cardiac Fibroblasts and Cardiomyocytes in Health and Disease
Caitlin Hall1, Katja Gehmlich1,2, Chris Denning3
1Institute of Cardiovascular Sciences University of Birmingham United Kingdom.
Insights
Cardiac fibroblasts are key to heart repair but can cause disease. This review explores their transition to myofibroblasts and communication with heart cells, impacting cardiac remodeling.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Fibrosis Research
Background:
- Cardiac fibroblasts are crucial for extracellular matrix deposition and myocardial support.
- Excessive fibroblast activation drives pathological cardiac remodeling, heart failure, and arrhythmias.
- Understanding fibroblast behavior is vital for treating cardiac diseases.
Purpose of the Study:
- To review the fibroblast-to-myofibroblast transition in the heart.
- To examine the crosstalk between cardiac fibroblasts and myocytes.
- To discuss current models for studying cardiac fibroblasts.
Main Methods:
- Literature review of cardiac fibroblast research.
- Analysis of fibroblast activation and proliferation mechanisms.
- Examination of fibroblast-myocyte interactions.
Main Results:
- Fibroblast activation and transition to myofibroblasts are central to cardiac fibrosis.
- Cardiac fibroblasts significantly influence cardiac myocyte function.
- Complex signaling pathways mediate fibroblast-myocyte crosstalk.
Conclusions:
- The fibroblast-to-myofibroblast transition is a critical process in cardiac remodeling.
- Interactions between fibroblasts and myocytes are key determinants of heart function.
- Further research into cardiac fibroblast behavior and therapeutic targeting is warranted.
Abstract:
Cardiac fibroblasts are the primary cell type responsible for deposition of extracellular matrix in the heart, providing support to the contracting myocardium and contributing to a myriad of physiological signaling processes. Despite the importance of fibrosis in processes of wound healing, excessive fibroblast proliferation and activation can lead to pathological remodeling, driving heart failure and the onset of arrhythmias. Our understanding of the mechanisms driving the cardiac fibroblast activation and proliferation is expanding, and evidence for their direct and indirect effects on cardiac myocyte function is accumulating. In this review, we focus on the importance of the fibroblast-to-myofibroblast transition and the cross talk of cardiac fibroblasts with cardiac myocytes. We also consider the current use of models used to explore these questions.
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