ArticleAging2024
CRYAB suppresses ferroptosis and promotes osteogenic differentiation of human bone marrow stem cells via binding and stabilizing FTH1.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- GFRα2 identified in TBI-induced bone healing is a novel therapeutic target for osteoporosis via osteogenesis and angiogenesis.Journal of orthopaedic translation · 2026Article
- Heat shock protein-mediated remodeling of the bone immune microenvironment: mechanisms and precision therapeutic strategies for osteoporosis.Journal of translational medicine · 2026Review
- Lactylation: a promising target for musculoskeletal disorders via interactions with chronic inflammation.Journal of advanced research · 2026Review
- Targeting Ferroptosis With Natural Products for the Treatment of Skeletal System Disease: An Updated Review.Journal of cellular and molecular medicine · 2026Review
- FAM96A functions as a novel pace controller for iron uptake to maintain iron homeostasis and erythropoiesis.Cell death and differentiation · 2026Article
- Targeting post-translational modifications: novel insights into bone metabolic diseases.Journal of advanced research · 2026Review
- Lactylation‑mediated ferroptosis: A novel mechanism and therapeutic prospects in human diseases (Review).International journal of molecular medicine · 2026Review
- 3D-printed magnetic scaffolds promote bone and vessel regeneration through CRYAB/PI3K-AKT and NF-κB pathways identified by proteomics.Bioactive materials · 2026Article
- Early detection of aberrant cell fate and repair using circulating progenitor cells in patients with heterotopic ossification.Nature communications · 2026Article
- Cellular mechanisms of osteoporosis: A comprehensive perspective on ferroptosis, cuproptosis and lipid metabolism abnormalities.Biomaterials translational · 2026Review
- The estrogen-ferroptosis axis in postmenopausal osteoporosis, osteoarthritis, and intervertebral disc degeneration: shared mechanisms and emerging evidence.Frontiers in immunology · 2026Review
- Post-translational modifications in ferroptosis: mechanisms and therapeutic potential.International journal of biological sciences · 2026Review
- Overcoming BET-inhibitor JQ1 resistance in aggressive non-small cell lung cancer by inducing ferroptosis via inhibition of the BRD2-FTH1 axis.The FEBS journal · 2025Article
- 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
- Activation of AKT1 enhances the capacity of senescent BMSCs to regulate osteoclast activation.Molecular medicine reports · 2025Article
- Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells.Cell death discovery · 2025Article
- Expression characteristics and biological significance of exosome-related genes in lung cancer.Discover oncology · 2025Article
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Endothelial-mesenchymal crosstalk drives osteogenic differentiation of human osteoblasts through Notch signaling.Cell communication and signaling : CCS · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone formation and homeostasis are greatly dependent on the osteogenic differentiation of human bone marrow stem cells (BMSCs). Therefore, revealing the mechanisms underlying osteogenic differentiation of BMSCs will provide new candidate therapeutic targets for osteoporosis.
methodsThe osteogenic differentiation of BMSCs was measured by analyzing ALP activity and expression levels of osteogenic markers. Cellular Fe and ROS levels and cell viability were applied to evaluate the ferroptosis of BMSCs. qRT-PCR, Western blotting, and co-immunoprecipitation assays were harnessed to study the molecular mechanism.
resultsThe mRNA level of CRYAB was decreased in the plasma of osteoporosis patients. Overexpression of CRYAB increased the expression of osteogenic markers including OCN, OPN, RUNX2, and COLI, and also augmented the ALP activity in BMSCs, on the contrary, knockdown of CRYAB had opposite effects. IP-MS technology identified CRYAB-interacted proteins and further found that CRYAB interacted with ferritin heavy chain 1 (FTH1) and maintained the stability of FTH1 via the proteasome mechanism. Mechanically, we unraveled that CRYAB regulated FTH1 protein stability in a lactylation-dependent manner. Knockdown of FTH1 suppressed the osteogenic differentiation of BMSCs, and increased the cellular Fe and ROS levels, and eventually promoted ferroptosis. Rescue experiments revealed that CRYAB suppressed ferroptosis and promoted osteogenic differentiation of BMSCs via regulating FTH1. The mRNA level of FTH1 was decreased in the plasma of osteoporosis patients.
conclusionsDownregulation of CRYAB boosted FTH1 degradation and increased cellular Fe and ROS levels, and finally improved the ferroptosis and lessened the osteogenic differentiation of BMSCs.
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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 Socratic graph.