Observational studyAging2021
Hepcidin-induced reduction in iron content and PGC-1β expression negatively regulates osteoclast differentiation to play a protective role in postmenopausal osteoporosis.
Observational study in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Advances in research on the relationship between mitochondrial dysfunction and osteoporosis: a bibliometric study from 2014 to 2024.Frontiers in medicine · 2025Pooled it
- Curcumin Alleviates the Osteogenesis Inhibition and the Aging Process in BMSCs Induced by Iron Overload Through Activating the NRF2/GPX4 Pathway.Phytotherapy research : PTR · 2026Article
- Mitigating mitochondrial dysfunction: a novel strategy for Chinese botanical drugs against osteoporosis.Frontiers in pharmacology · 2026Review
- Ferroptosis in compromised bone healing after trauma: from the iron/ROS microenvironment to non-union and bone defect reconstruction.Frontiers in medicine · 2026Review
- Spermidine prevents iron overload-induced impaired bone mass by activating SIRT1/SOD2 signaling in senile rat model.Redox report : communications in free radical research · 2025Article
- Hepcidin knockout exacerbates hindlimb unloading-induced bone loss in mice through inhibiting osteoblastic differentiation.BMC musculoskeletal disorders · 2025Article
- Role of sirtuins in obesity and osteoporosis: molecular mechanisms and therapeutic targets.Cell communication and signaling : CCS · 2025Review
- Ferroptosis and bone health: bridging the gap between mechanisms and therapy.Frontiers in immunology · 2025Review
- The role of ferroptosis in osteoporosis: from pathogenic mechanisms to natural product-driven therapeutic innovations.Frontiers in medicine · 2025Review
- Arctiin alleviates knee osteoarthritis by suppressing chondrocyte oxidative stress induced by accumulated iron via AKT/NRF2/HO-1 signaling pathway.Scientific reports · 2024Article
- Repair and regeneration: ferroptosis in the process of remodeling and fibrosis in impaired organs.Cell death discovery · 2024Review
- Irisin Protects Musculoskeletal Homeostasis via a Mitochondrial Quality Control Mechanism.International journal of molecular sciences · 2024Review
- HAMP predicts a pivotal role in modulating the malignant behaviors of non-small cell lung cancer cells.Aging · 2024Article
- No genetic causal association between iron status and pulmonary artery hypertension: Insights from a two-sample Mendelian randomization.Pulmonary circulation · 2024Article
- Ferroptosis in Osteocytes as a Target for Protection Against Postmenopausal Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of Iron Accumulation in Osteoporosis and the Underlying Mechanisms.Current medical science · 2023Article
- Construction of ceRNA regulatory networks for osteoporosis.Molecular medicine reports · 2023Article
- The Role of Trace Elements and Minerals in Osteoporosis: A Review of Epidemiological and Laboratory Findings.Biomolecules · 2023Review
- A dual functional Ti-Ga alloy: inhibiting biofilm formation and osteoclastogenesis differentiation via disturbing iron metabolism.Biomaterials research · 2023Article
- Fighting age-related orthopedic diseases: focusing on ferroptosis.Bone research · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a necessary trace element, iron is involved in many physiological processes. Clinical and basic studies have found that disturbances in iron metabolism, especially iron overload, might lead to bone loss and even be involved in postmenopausal osteoporosis. Hepcidin is a key regulator of iron homeostasis. However, the exact role of hepcidin in bone metabolism and the underlying mechanism remain unknown. In this study, we found that in postmenopausal osteoporosis cohort, the concentration of hepcidin in the serum was significantly reduced and positively correlated with bone mineral density. Ovariectomized (OVX) mice were then used to construct an osteoporosis model. Hepcidin overexpression in these mice significantly improved bone mass and rescued the phenotype of bone loss. Additionally, overexpression of hepcidin in OVX mice greatly reduced the number and differentiation of osteoclasts
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.