Mitochondrial dysfunction and mitochondrial therapies in heart failure

Cardiovascular diseases remain the leading cause of death worldwide in the last decade, accompanied by immense health and economic burdens. Heart failure (HF), as the terminal stage of many cardiovascular diseases, is a common, intractable, and costly medical condition. Despite significant improvements in pharmacologic and device therapies over the years, life expectancy for this disease remains poor. Current therapies have not reversed the trends in morbidity and mortality as expected. Thus, there is an urgent need for novel potential therapeutic agents. Although the pathophysiology of the failing heart is extraordinarily complex, targeting mitochondrial dysfunction can be an effective approach for potential treatment. Increasing evidence has shown that mitochondrial abnormalities, including altered metabolic substrate utilization, impaired mitochondrial oxidative phosphorylation (OXPHOS), increased reactive oxygen species (ROS) formation, and aberrant mitochondrial dynamics, are closely related to HF. Here, we reviewed the findings on the role of mitochondrial dysfunction in HF, along with novel mitochondrial therapeutics and their pharmacological effects.