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Published on: March 19, 2013
Therapeutic targets for cardiac fibrosis: from old school to next-gen
Insights
Cardiovascular diseases involve cardiac fibrosis driven by myofibroblasts. Targeting epigenetic regulators offers novel therapeutic strategies to combat heart failure and related conditions.
Area of Science:
- Cardiovascular Medicine
- Fibrosis Research
- Epigenetics
Background:
- Cardiovascular diseases are the leading global cause of death.
- Pathological cardiac fibrosis, mediated by myofibroblasts, underlies cardiac dysfunction and heart failure.
- Current treatments targeting cardiac fibroblasts and fibrosis are limited.
Purpose of the Study:
- To review classical regulators of cardiac fibrosis.
- To highlight emerging epigenetic targets for therapeutic intervention.
- To explore novel strategies for mitigating myofibroblast activation and cardiac fibrosis.
Main Methods:
- Literature review of classical fibrosis regulators.
- Analysis of emerging epigenetic mechanisms in cardiac fibrosis.
- Discussion of therapeutic potential for cardiovascular diseases.
Main Results:
- Myofibroblast activation is a key factor in fibrotic remodeling.
- Epigenetic modifications represent promising targets for antifibrotic therapies.
- Targeting fibrosis could treat diverse heart conditions.
Conclusions:
- Novel epigenetic strategies hold potential to revolutionize cardiovascular disease treatment.
- Mitigating cardiac fibrosis offers a promising therapeutic avenue for heart failure and related conditions.
- Further research into epigenetic regulators is crucial for developing effective antifibrotic therapies.
Abstract:
Cardiovascular diseases remain the leading cause of death worldwide, with pathological fibrotic remodeling mediated by activated cardiac myofibroblasts representing a unifying theme across etiologies. Despite the profound contributions of myocardial fibrosis to cardiac dysfunction and heart failure, there currently exist limited clinical interventions that effectively target the cardiac fibroblast and its role in fibrotic tissue deposition. Exploration of novel strategies designed to mitigate or reverse myofibroblast activation and cardiac fibrosis will likely yield powerful therapeutic approaches for the treatment of multiple diseases of the heart, including heart failure with preserved or reduced ejection fraction, acute coronary syndrome, and cardiovascular disease linked to type 2 diabetes. In this Review, we provide an overview of classical regulators of cardiac fibrosis and highlight emerging, next-generation epigenetic regulatory targets that have the potential to revolutionize treatment of the expanding cardiovascular disease patient population.
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