Therapeutic targets for cardiac fibrosis: from old school to next-gen

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.

Automated summary

Cardiovascular diseases are the leading cause of death worldwide, with myocardial fibrosis playing a significant role in cardiac dysfunction and heart failure. However, current clinical interventions targeting cardiac fibroblasts and fibrotic tissue deposition are limited. Exploring novel strategies to mitigate or reverse myofibroblast activation and cardiac fibrosis can potentially revolutionize treatment for various heart diseases.