The Role of Mitochondrial Dysfunction in Heart Failure and Potential Therapeutic Targets

Abstract

Advances in pharmacotherapy as well as device therapy in common cardiovascular diseases, especially implementation of rapid coronary reperfusion as a key management strategy in acute ischemic disease, improved overall survival. Yet, this success contributes to increased number of patients susceptible to heart failure development due to damaged myocardium. Although survival after heart failure diagnosis has improved over time, the death rate remains high: ≈50% of people diagnosed with this disease will die within 5 years. Thus, not only there is a space for novel concepts and strategies in the treatment of symptomatic heart failure, but also they are urgently needed. The mechanisms underlying the development of heart failure are multiple, complex, and not well understood. However, regardless of the cause of heart failure, or whether its presentation is acute or chronic, altered mitochondrial function/bioenergetics appears to play a substantial role in its pathophysiology. As such, the mitochondria are potentially promising, but still underused, target for new HF therapies. This review will focus on changes that occur in the mitochondria of failing myocardium, as well as on targets and approaches that suggest potential therapeutic effect in this ominous disease.