Commentary 10.1172/JCI147072
1West China Hospital of Stomatology, Sichuan University, Chengdu, China.
2Maine Medical Center Research Institute, Scarborough, Maine, USA.
Address correspondence to: Clifford J. Rosen, 81 Research Drive, Scarborough, Maine 04074, USA. Email: rosenc@mmc.org.
Find articles by Liu, H. in: JCI | PubMed | Google Scholar
1West China Hospital of Stomatology, Sichuan University, Chengdu, China.
2Maine Medical Center Research Institute, Scarborough, Maine, USA.
Address correspondence to: Clifford J. Rosen, 81 Research Drive, Scarborough, Maine 04074, USA. Email: rosenc@mmc.org.
Find articles by Rosen, C. in: JCI | PubMed | Google Scholar
Published March 1, 2021 - More info
The involvement of nitric oxide (NO) in preventing bone loss has long been hypothesized, but despite decades of research the mechanisms remain obscure. In this issue of the JCI, Jin et al. explored NO deficiency using human cell and mouse models that lacked argininosuccinate lyase (ASL), the enzyme involved in synthesizing arginine and NO production. Osteoblasts that did not express ASL produced less NO and failed to differentiate. Notably, in the context of Asl deficiency, heterozygous deletion of caveolin 1, which normally inhibits NO synthesis, restored NO production, osteoblast differentiation, glycolysis, and bone mass. These experiments suggest that ASL regulates arginine synthesis in osteoblasts, which leads to enhanced NO production and increased glucose metabolism. After a period when research slowed, these studies, like the legendary phoenix, renew the exploration of NO in bone biology, and provide exciting translational potential.
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