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Updated: Aug 18, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
The cardiac fibroblast: therapeutic target in myocardial remodeling and failure
R Dale Brown1, S Kelly Ambler, M Darren Mitchell
1Division of Cardiology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. Dale.Brown@uchsc.edu
Insights
Cardiac fibroblasts are key to heart health and disease. Targeting these cells offers new therapeutic strategies for heart failure and myocardial remodeling.
Area of Science:
- Cardiovascular Biology
- Fibrosis Research
- Pharmacology
Background:
- Cardiac fibroblasts are crucial for extracellular matrix maintenance in healthy hearts.
- They mediate inflammatory and fibrotic remodeling in injured or failing hearts.
Purpose of the Study:
- To evaluate cardiac fibroblasts as a therapeutic target in heart disease.
- To discuss fibroblast cell biology in normal and pathological cardiac function.
- To review drug therapies targeting cardiac fibroblasts.
Main Methods:
- Literature review of cardiac fibroblast biology.
- Analysis of cardiac fibrosis as a risk factor in heart failure.
- Summary of candidate drug therapies acting on cardiac fibroblasts.
Main Results:
- Cardiac fibroblasts' unique biology influences cardiac function.
- Cardiac fibrosis is an independent risk factor for heart failure outcomes.
- Several drug classes show potential therapeutic benefit by targeting fibroblasts.
Conclusions:
- Cardiac fibroblasts represent a promising therapeutic target for heart disease.
- Future research should focus on cardiac fibroblast biology and pharmacotherapy.
- Targeting fibroblasts may improve outcomes in heart failure and myocardial remodeling.
Abstract:
Cardiac fibroblasts play a central role in the maintenance of extracellular matrix in the normal heart and as mediators of inflammatory and fibrotic myocardial remodeling in the injured and failing heart. In this review, we evaluate the cardiac fibroblast as a therapeutic target in heart disease. Unique features of cardiac fibroblast cell biology are discussed in relation to normal and pathophysiological cardiac function. The contribution of cardiac fibrosis as an independent risk factor in the outcome of heart failure is considered. Candidate drug therapies that derive benefit from actions on cardiac fibroblasts are summarized, including inhibitors of angiotensin-aldosterone systems, endothelin receptor antagonists, statins, anticytokine therapies, matrix metalloproteinase inhibitors, and novel antifibrotic/anti-inflammatory agents. These findings point the way to future challenges in cardiac fibroblast biology and pharmacotherapy.
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