Researchers at Helmholtz Munich have discovered a new use for vitamin K, often recognized for its role in blood clotting. The scientists found that vitamin K in its fully reduced form functions as an antioxidant by effectively preventing ferroptotic cell death. Cellular iron plays a significant role in the natural cell death process known as ferroptosis, which is also characterized by the oxidative breakdown of cellular membranes. Additionally, the scientists determined that FSP1 is the long-suspected but unidentified warfarin-insensitive enzyme lowering vitamin K.
In recent years, ferroptosis has been linked to several illnesses, including Alzheimer’s disease and acute organ damage. Thus, the current findings suggest that vit. K therapy may be a fresh, effective method for treating these ferroptosis-related disorders.
A Powerful Ferroptosis Suppressant
The inhibition of ferroptosis is seen to be a very promising strategy for treating many degenerative diseases, hence research into new mechanisms and substances that control ferroptosis is ongoing. Researchers from Tohoku University (Japan), University of Ottawa (Canada), and Technical University of Dresden (Germany), under the direction of Dr. Eikan Mishima and Dr. Marcus Conrad, both from the Institute of Metabolism and Cell Death at Helmholtz Munich, thoroughly examined several naturally occurring vitamins and their derivatives to identify these new molecules. Dr. Eikan Mishima, the study’s first author, said, “Surprisingly, we identified that vit. K, including phylloquinone (vitamin K1) and menaquinone-4 (vitamin K2), can efficiently rescue cells and tissues from undergoing ferroptosis”
FSP1, a Highly Regarded Vitamin K Reducing Enzyme, Is Being Revealed.
Ferroptosis suppressor protein-1, also known as FSP1, was discovered as a new and potent regulator of ferroptosis by a research team led by Dr. Marcus Conrad in 2019. The study team has found that vitamin K hydroquinone, which has been reduced, functions as a potent lipophilic antioxidant and inhibits ferroptosis by capturing oxygen radicals in lipid bilayers. Furthermore, they discovered that FSP1 is the enzyme responsible for effectively reducing vit. K to vit. K hydroquinone, resulting in the activation of a brand-new, non-canonical vit. K cycle. The team went on to demonstrate that FSP1 is responsible for the vitamin K-reduction pathway being insensitive to warfarin, one of the most widely prescribed anticoagulants, given that vitamin K plays a crucial role in blood coagulation processes.
New Insights Into the Metabolism of Vitamin K
The final mystery surrounding vitamin K metabolism in blood clotting was resolved by identifying this enzyme, and the chemical basis for why vit. K serves as the antidote for warfarin overdose was clarified. As a result, Dr. Marcus Conrad explained that the findings link the two fields of ferroptosis research and vit. K biology and will serve as the foundation for the development of novel treatment options for disorders where ferroptosis has been involved. The researchers also postulate that vit. K may be one of the oldest forms of naturally occurring antioxidants because ferroptosis is most likely one of the oldest types of cell death. So, new facets of vitamin K’s function in life’s evolution are anticipated to emerge, according to Dr. Marcus Conrad
