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Published on: June 14, 2016
Antifibrotic therapies to control cardiac fibrosis
1Department of Materials Science and Engineering, The Ohio State University, 2041 College Road, Columbus, OH 43210 USA.
Insights
Cardiac fibrosis after heart attack worsens heart function and leads to heart failure. New therapies targeting myofibroblasts show promise in preventing this progression and improving cardiac health.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Biomaterials Science
Background:
- Cardiac fibrosis is a natural response to myocardial infarction, but its progression impairs heart function and can lead to heart failure.
- Myofibroblasts are key drivers of cardiac fibrosis, originating from various cell types and stimulated by growth factors like TGF-β.
- Current therapeutic strategies for cardiac fibrosis are limited, highlighting the need for effective interventions.
Purpose of the Study:
- To review current advancements in therapeutic approaches for inhibiting cardiac fibrosis progression.
- To explore strategies targeting myofibroblast formation and activity.
- To discuss the potential of localized delivery systems for antifibrotic therapies.
Main Methods:
- Review of existing literature on cardiac fibrosis and therapeutic interventions.
- Analysis of studies involving systemic and localized drug delivery.
- Examination of cell-based therapies and biomaterial applications.
Main Results:
- Myofibroblast inhibition strategies have shown efficacy in preventing cardiac fibrosis.
- Localized delivery of antifibrotic drugs and biomaterials offers promising therapeutic potential.
- Cell-based therapies, when combined with biomaterials, represent an emerging treatment avenue.
Conclusions:
- Inhibiting myofibroblast formation is crucial for preventing cardiac fibrosis progression post-myocardial infarction.
- Localized therapeutic delivery systems, including biomaterials and cell-based approaches, are key areas for future development.
- Further research is needed to establish efficient and safe therapeutic strategies to combat cardiac fibrosis and prevent heart failure.
Abstract:
Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation, and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-β), angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. This review addresses current progresses in cardiac fibrosis therapies.
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