Itaconate is a metabolic regulator of bone formation in homeostasis and arthritis
Authors' conclusion
In summary, we identify itaconate, generated as a result of the metabolic rewiring during osteoclast differentiation, as a previously unrecognised regulator of osteoblasts.
Study context
- Population
- Cells during osteoclast and osteoblast generation; Irg1-deficient mice in inflammatory or non-inflammatory models of bone loss
Methodological detailsin vitro and in vivo, murine and human cells, Irg1-deficient mice
- In vitro and in vivo
- Murine and human cells
- Irg1-deficient mice
Main finding
As reported in the abstract
- Preosteoclasts rearrange their tricarboxylic acid cycle during differentiation, depending on both glucose and glutamine, with induction of Irg1 and production of itaconate
- IRG1-itaconate axis dispensable for osteoclast generation in vitro and in vivo
- Itaconate accelerates osteogenic differentiation in human and murine cells, with reduced proliferation and altered metabolism
- Itaconate supplementation increases bone formation by boosting osteoblast activity in mice
- Irg1-deficient mice exhibit decreased bone mass and reduced osteoproliferative lesions in experimental arthritis
Original publication
Itaconate is a metabolic regulator of bone formation in homeostasis and arthritis. Ann Rheum Dis. Published 21 October 2024. doi:10.
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