Targeting mitochondrial dynamics: An attractive therapeutic approach for treating cardiovascular diseases

Despite dramatic enhancement of therapeutic strategies in cardiovascular pathophysiology, heart diseases remain a challenging health issue worldwide and are a leading cause of mortality and morbidity. This highlights the necessity for novel therapeutic targets to be identified.

The mitochondria are considered to be the "powerhouses" of the cell as they are responsible for the generation of energy in eukaryotic cells. Beyond their role in energy production, they are also involved in several processes such as innate immunity, autophagy, redox signaling, calcium homeostasis, and stem cells reprogramming. Mitochondria are dynamic organelles with the ability to change their shape by undergoing fusion to generate elongated interconnected mitochondrial networks, and fission to produce discrete fragmented mitochondria. These processes are regulated by mitochondrial fusion and fission proteins, which are essential for maintaining the mitochondrial balance.

Over the past decade, the importance of mitochondria in cardiovascular pathophysiology has been given much attention. Changes in mitochondrial dynamics have been associated with the development of various cardiac diseases that includes ischemia-reperfusion (I/R) injury and cardiac hypertrophy and heart failure (HF)

In this work we study the interaction between two mitochondrial quality control proteins. Using rational design, we develop peptides that interfere specifically with their protein-protein interactions and investigate the effect of the peptides on oxygen-starved cardiac cells. These studies may pave the way for development of novel pharmacological tools for treating heart failure.