About this activity
Abstract
Discussion Forum (0)
Bone is a highly dynamic tissue, and its functional properties are maintained by an intricate cellular interplay between growth plate chondrocytes, bone-forming osteoblasts and bone-resorbing osteoclasts. The notion that skeletal cell biology is controlled not only by cytokines and hormonal signaling, but also by specific metabolic programs has gained significant traction in recent years. These metabolic pathways are linked to typical cellular functions, including survival, proliferation and matrix production, and may thus differ depending on the differentiation status. In addition, skeletal cell metabolism is likely controlled by cell-intrinsic factors and is modified by growth factors and hormones. While most attention has been given to glucose metabolism and glucose-fueled pathways, our recent work has also revealed a major regulatory role for amino acid metabolism. In my talk, I will discuss how glutamine, the most abundant circulating amino acid, controls chondrocyte identity and function during endochondral ossification and bone repair. In addition, I will highlight the importance of de novo serine synthesis to support chondrocyte anabolism in the developing growth plate and during fracture healing. Finally, I will provide insight on how dysregulated amino acid metabolism is linked to skeletal pathology, thereby suggesting that targeting specific metabolic pathways may hold therapeutic potential.
Coming soon!
Coming soon!
The metabolic needs of healthy and diseased skeletal cells
Steve Stegen
About this activity
Abstract
Discussion Forum (0)
Bone is a highly dynamic tissue, and its functional properties are maintained by an intricate cellular interplay between growth plate chondrocytes, bone-forming osteoblasts and bone-resorbing osteoclasts. The notion that skeletal cell biology is controlled not only by cytokines and hormonal signaling, but also by specific metabolic programs has gained significant traction in recent years. These metabolic pathways are linked to typical cellular functions, including survival, proliferation and matrix production, and may thus differ depending on the differentiation status. In addition, skeletal cell metabolism is likely controlled by cell-intrinsic factors and is modified by growth factors and hormones. While most attention has been given to glucose metabolism and glucose-fueled pathways, our recent work has also revealed a major regulatory role for amino acid metabolism. In my talk, I will discuss how glutamine, the most abundant circulating amino acid, controls chondrocyte identity and function during endochondral ossification and bone repair. In addition, I will highlight the importance of de novo serine synthesis to support chondrocyte anabolism in the developing growth plate and during fracture healing. Finally, I will provide insight on how dysregulated amino acid metabolism is linked to skeletal pathology, thereby suggesting that targeting specific metabolic pathways may hold therapeutic potential.
Coming soon!
Coming soon!
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