Increasing evidence indicates that disruption of mitochondrial function may be important in the development and progression of many metabolic diseases. Mitochondrial dysfunction occurs following inhibition of oxidative phosphorylation, which results in decreased ATP production, loss of mitochondrial potential, increased reactive oxygen species (ROS) and, ultimately, redistribution of mitochondrial cell death proteins.

 

Emerging evidence also suggests that the endocannabinoid system can modulate mitochondrial integrity and function. Endocannabinoids, via activation of CB1 receptors, are known to impair mitochondrial respiration, morphology and physiology, and CB1 receptor blockade improves mitochondrial oxidative phosphorylation, biogenesis, integrity and membrane physiology.

 

Our goal is to uncover a new role for CB1 receptor as a modulator of mitochondrial function in different metabolic diseases by regulating mitochondrial biogenesis, integrity, and membrane physiology.