Inhibition of Oxytosis/Ferroptosis by Cannabinol Requires Mitochondria and is Independent of Cannabinoid Receptors

Dr. Pam Maher, from the The Salk Institute for Biological Studies, USA will join us this year to present her most recent findings on "Inhibition of oxytosis/ferroptosis by cannabinol requires mitochondria and is independent of cannabinoid receptors".

The oxytosis/ferroptosis regulated cell death pathway recapitulates many features of mitochondrial dysfunction associated with the aging brain and has emerged as a potential key mediator of neurodegeneration. It has thus been proposed that the oxytosis/ferroptosis pathway can be used to identify novel drug candidates for the treatment of age-associated neurodegenerative diseases that act by preserving mitochondrial function. Previously, we identified cannabinol (CBN) as a potent neuroprotector.

Here, Dr. Maher demonstrates that not only does CBN protect nerve cells from oxytosis/ferroptosis in a manner that is dependent on mitochondria, it does so independently of cannabinoid receptors.

Specifically, CBN directly targets mitochondria and preserves key mitochondrial functions including redox regulation, calcium uptake, membrane potential, bioenergetics, biogenesis, and modulation of fusion/fission dynamics that are disrupted following induction of oxytosis/ferroptosis.

These protective effects of CBN are at least partly mediated by the promotion of endogenous antioxidant defenses and the activation of AMP-activated protein kinase (AMPK) signaling.

Together, her data highlight the potential of mitochondrially-targeted compounds such as CBN as novel oxytotic/ferroptotic inhibitors to rescue mitochondrial dysfunction as well as opportunities for the discovery and development of future neurotherapeutics.

Polyphenols Applications 2022 Congress
September 28-30, 2022 - Valencia, Spain
www.polyphenols-site.com