ArticleCell death & disease2023
REPIN1 regulates iron metabolism and osteoblast apoptosis in osteoporosis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Cross-ancestry genome-wide association study identifies new susceptibility genes for preeclampsia.BMC pregnancy and childbirth · 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
- FTMT-mediated suppression of mitophagy links iron accumulation to osteoporosis.Redox biology · 2026Article
- LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism.Cell death & disease · 2026Article
- m6A RNA modifications in neurosystem genes as early markers for osteoporosis with iron accumulation.Molecular biology reports · 2026Article
- Dysregulation of the immune microenvironment in essential thrombocythemia: the interplay of core genes and inflammation-related signaling pathways.Frontiers in immunology · 2026Article
- Hyperoside promotes osteoblast differentiation by increasing osteoclast-derived migrasomes to alleviate osteoporosis.American journal of translational research · 2026Article
- Programmed cell death in degenerative skeletal diseases: molecular crosstalk and combinatorial therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Research progress on mitochondria in bone defect repair: mechanisms and therapeutic implications.Frontiers in bioengineering and biotechnology · 2026Review
- Targeting ferroptosis to rescue osteogenic differentiation in BRONJ-affected jawbone mesenchymal stem cells: the role of miR-145-3p and exosome-mediated therapy.Journal of nanobiotechnology · 2025Article
- Research on the role and mechanism of the PI3K/Akt/mTOR signalling pathway in osteoporosis.Frontiers in endocrinology · 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
- Lipocalin-2 and intestinal diseases.World journal of gastroenterology · 2024Review
- [Research progress on iron metabolism in the occurrence and development of periodontitis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Review
- Metal ion metabolism and osteoporosis: possible implications for pharmaceutical biotechnology and tissue engineering.Science China. Life sciences · 2024Article
- M1 macrophage-derived exosomes promote intervertebral disc degeneration by enhancing nucleus pulposus cell senescence through LCN2/NF-κB signaling axis.Journal of nanobiotechnology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is not well treated due to the difficulty of finding commonalities between the various types of it. Iron homeostasis is a vital component in supporting biochemical functions, and iron overload is recognized as a common risk factor for osteoporosis. In this research, we found that there is indeed evidence of iron accumulation in the bone tissue of patients with osteoporosis and REPIN1, as an origin specific DNA binding protein, may play a key role in this process. We revealed that sh-Repin1 therapy can rescue bone loss in an iron-overload-induced osteoporosis mouse model. Knockdown of Repin1 can inhibit apoptosis and enhance the resistance of osteoblasts to iron overload toxicity. REPIN1 promoted apoptosis by regulating iron metabolism in osteoblasts. Mechanistically, knockdown of Repin1 decreased the expression of Lcn2, which ameliorated the toxic effects of intracellular iron overload. The anti-iron effect of lentivirus sh-Repin1 was partially reversed or replicated by changing LCN2 expression level via si-RNA or plasmid, which indirectly verified the key regulatory role of LCN2 as a downstream target. Furthermore, the levels of BCL2 and BAX, which play a key role in the mitochondrial apoptosis pathway, were affected. In summary, based on the results of clinical specimens, animal models and in vitro experiments, for the first time, we proved the key role of REPIN1 in iron metabolism-related osteoporosis.
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