Ferron Team Identifies Vitamin K GAS6-TAM Bone Pathway in 6-Month Mice
Updated
Updated · SciTechDaily · Jun 13
Ferron Team Identifies Vitamin K GAS6-TAM Bone Pathway in 6-Month Mice
1 articles · Updated · SciTechDaily · Jun 13
Summary
Male mice lacking γ-glutamyl carboxylase in osteoblasts developed higher bone mass by 6 months because bone resorption fell, not because bone formation increased.
The team traced that effect to GAS6, a vitamin K-dependent signal released by osteoblasts that activates AXL and MerTK receptors on pre-osteoclasts, driving their fusion into larger bone-resorbing cells.
Blocking AXL and MerTK sharply reduced osteoclast production in lab experiments, while transgenic mice with elevated GAS6 showed lower bone density, more osteoclasts and higher resorption.
Published in Bone Research, the study offers a mechanism for vitamin K's long-noted bone benefits and points to GAS6-TAM signaling as a potential target for osteoporosis and other high-resorption bone diseases.
A newly found vitamin K pathway promotes bone loss. Should we rethink our dietary advice for bone health?
Scientists have a new target for stopping bone loss. Could this finally lead to a cure for osteoporosis?
Vitamin K-Dependent GAS6–TAM Pathway: The 2026 Breakthrough Transforming Osteoporosis Treatment and Bone Remodeling Science
Overview
In 2026, Dr. Mathieu Ferron's team made a major breakthrough by uncovering a new vitamin K-dependent pathway that controls bone resorption. Their research showed that when the *Ggcx* gene was inactivated in osteoblasts—the cells that build bone—mice developed higher bone density and mass. This was because the number of osteoclasts, which break down bone, was reduced, leading to less bone resorption. The study revealed that osteoblasts lacking *Ggcx* could not support osteoclast formation effectively, offering a new understanding of how vitamin K shapes bone health and opening doors for better treatments for bone diseases.