Background: Mitochondria are cellular organelles responsible for energy production, calcium handling,
controlled synthesis of reactive oxygen species (ROS), and regulation of apoptosis. All these functions are
crucial for cardiac homeostasis, and may be impaired in chronic heart failure (CHF). Therefore, mitochondrial
dysfunction might represent a crucial element in the onset and progression of CHF and, as such, a promising
Methods: Original articles and review on the treatment of mitochondrial dysfunction in CHF were searched on
Medline and Scopus.
Results: The present review summarizes the current knowledge about mitochondrial modulation as a therapeutic
strategy for CHF, and proposes some perspectives for future studies. Mitochondrial dysfunction can be ascribed
to neuro-humoral activation and cardiac remodeling associated with CHF. Conceptually, the correction of mitochondrial
dysfunction could provide an additive benefit to optimal CHF treatment. Increasing glucose metabolism
and reducing oxidative stress within mitochondria are the two most promising approaches, even though further
studies are required before implementing new treatments in the setting of CHF. On the other hand, inhibition of
apoptosis, and normalization of calcium and mitochondrial dynamics have been assessed almost exclusively in ex
vivo models, and mostly in settings other than CHF.
Conclusion: Mitochondrial modulation in CHF is an intriguing example of translational research and a potentially