ArticleFrontiers in endocrinology2022
PTH 1-34 promoted bone formation by regulating iron metabolism in unloading-induced bone loss.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Prevalence of metabolic syndrome in patients with end-stage renal disease: a systematic review and meta-analysis.International urology and nephrology · 2024Pooled it
- Hepcidin knockout exacerbates hindlimb unloading-induced bone loss in mice through inhibiting osteoblastic differentiation.BMC musculoskeletal disorders · 2025Article
- PTH1R Suppressed Apoptosis of Mesenchymal Progenitors in Mandibular Growth.International journal of molecular sciences · 2024Article
- Restless leg syndrome as a complication of primary hyperparathyroidism: insights from a retrospective study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PTH 1-34 (teriparatide) is approved by FDA for the treatment of postmenopausal osteoporosis. Iron overload is a major contributing factor for bone loss induced by unloading. Whether iron metabolism is involved in the regulation of PTH 1-34 on unloading-induced osteoporosis has not yet been reported. Here, we found that PTH 1-34 attenuated bone loss in unloading mice. PTH 1-34 regulated the disturbance of iron metabolism in unloading mice by activating Nrf2 and further promoting hepcidin expression in the liver. In addition, the Nrf2 inhibitor selectively blocked hepcidin expression in the liver of unloading mice, which neutralized the inhibitory effect of PTH 1-34 on bone loss and the recovery of iron metabolism in unloading mice. Finally, we found that PTH 1-34 promoted the differentiation and inhibited apoptosis of osteoblasts by regulating iron metabolism and maintaining redox balance under unloading conditions. Our results suggested that PTH 1-34 promoted bone formation by regulating iron metabolism under unloading conditions.
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