Vitamin K-dependent processes linked to vascular calcification and oxidative stress

New research study once again links vitamin K2 benefits against calcification and free radical damage

Arteriosclerosis, Thrombosis, and Vascular Biology has published a new paper examining the well-known and alternative pathways of vitamin K, adding to the substantial argument that vitamin K2 can greatly impact cardiovascular health.

The paper was funded by a grant awarded to NattoPharma’s International Research Network by the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant.

“NattoPharma has a long history of funding research and participating in collaborative research such as was provided in the Horizon 2020 grant. The body of evidence supporting cardiovascular health benefits continues to grow and we believe will help expand both awareness and consumer demand for vitamin K2,” says NattoPharma CEO Kjetil Ramsøy.

Dr Hogne Vik, NattoPharma Chief Medical Officer, explains: “According to at least five different epidemiological studies, vitamin K2 – and not K1 – is cardioprotective. That is why the majority of new clinical trials, which are focused on cardiovascular health, are performed using K2 as MK-7."

"Moreover, vitamin K2 was shown to be not only more potent form than Vitamin K1, but also the compound that possesses additional biological activity (not present in the case of K1).”

Aortic aneurysm is a vascular disease whereby the ECM (extracellular matrix) of a blood vessel degenerates, leading to dilation and eventually vessel wall rupture. Recently, it was shown that calcification of the vessel wall is involved in both the initiation and progression of aneurysms.

To that end, the authors of the paper, “Role of Vascular Smooth Muscle Cell Phenotypic Switching and Calcification in Aortic Aneurysm Formation: Involvement of Vitamin K-Dependent Processes,” summarise the current literature on vascular smooth muscle cell phenotypic switching and vascular calcification in relation to aneurysm.

Moreover, they address the role of vitamin K and vitamin K-dependent proteins (VKDPs) that are involved in vascular calcification and aneurysm.

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The review highlighted well-known and alternative pathways of vitamin K activity:

  • vitamin K is known to activate matrix Gla Protein (MGP), by which it inhibits vascular calcification
  • vitamin K has the ability to scavenge free radicals, reduce oxidative stress, and decrease vascular calcification.

“Therefore, it is tempting to postulate that vitamin K deficiency plays a role in aneurysm formation,” the authors conclude. “Vitamin K supplementation holds the potential to lower the risk of aortic aneurysms and improve cardiovascular outcome."

The paper is significant because it continues to build upon the argument that vitamin K2 is an essential nutrient for protecting cardiovascular health, while also opening up new areas of benefits, according to Dr Vik.

“Once again, Vitamin K is known to activate MGP, which inhibits vascular calcification,” says Vik.

“This new paper also finds vitamin K has the ability to scavenge free radicals, reduce oxidative stress, and decrease calcification. We support the authors’ supposition that Vitamin K deficiency plays a role in aneurysm formation. Clearly, vitamin K2 supplementation holds the potential to lower the risk of aortic aneurysms and improve cardiovascular outcomes.”

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