ArticleRedox report : communications in free radical research2025
Neutrophil extracellular traps drive osteoporosis via NCF2-dependent signaling: integrated transcriptomics with mechanistic validation.
Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Natural Polysaccharide-Mediated Nano-Delivery Systems for Osteoporosis Therapy From a Gut-Bone Axis Regulatory Perspective.Advanced healthcare materials · 2026Review
- Integrative multi-omics analysis of growth plate regulation underlying body size in miniature pigs.Communications biology · 2026Article
- Neutrophil extracellular traps in osteoporosis: mechanistic links to bone remodeling imbalance and therapeutic perspectives.Molecular biology reports · 2026Review
- Diabetes Mellitus Facilitates Gallstone Formation Through CXCR2-NETs-Mediated Liver-Bile Barrier Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Vascular Non-Inflammatory Molecule-1 Aggravates Acute Kidney Injury Induced Acute Lung Injury Via Promoting Neutrophil Extracellular Traps Formation.Inflammation · 2026Article
- Targeting innate immunity to modulate bone metabolism: a novel strategy for osteoporosis treatment.Frontiers in aging · 2026Review
- Development and evaluation of a machine learning based risk prediction model for osteoporosis.Frontiers in molecular biosciences · 2026Article
- Clinically constrained Bayesian network analysis of immune-metabolic factors associated with bone mineral density in a real-world orthopedic cohort.Frontiers in surgery · 2026Article
- Senescent immune cells, inflammaging, and bone loss: therapeutic potential and translational challenges of senolytics in osteoporosis.Frontiers in endocrinology · 2026Review
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Authors and funding
11 authors.
Funding
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Abstract
backgroundInflammation and immune responses play key roles in osteoporosis (OP) pathogenesis. Osteoimmunology highlights immune dysregulation as a significant contributor to OP, but the specific biological mechanisms linking immune dysfunction to bone loss remain unclear. Understanding these mechanisms is essential for targeted therapies.
methodsWe established a rat OP model via bilateral ovariectomy. Transcriptomic sequencing (RNA-seq) identified differentially expressed genes (DEGs), and summary data-based Mendelian randomization (SMR) analysis validated their causal associations with OP. Primary neutrophils isolated from bone marrow and differentiated HL-60 neutrophil-like cells were induced to form neutrophil extracellular traps (NETs), and siRNA was employed to knock down the NCF2 gene. Conditioned media from these neutrophils were subsequently applied to primary osteoblasts to evaluate effects on osteogenic differentiation.
resultsRNA-seq identified 4,497 DEGs (1,606 upregulated, 2,891 downregulated) in OP rats, significantly enriched in immune response and NETs formation pathways. NETs markers (NE, MPO, CitH3) were markedly elevated in OP bone tissue and stimulated neutrophils. SMR analysis identified VDAC1, PLCG2, and NCF2 as key genes significantly associated with OP risk, experimentally validated at the tissue and cellular levels. Knockdown of NCF2 reduced NETs formation in neutrophil-like cells and alleviated NETs-induced osteoblast differentiation impairment. Drug prediction and molecular docking analyses demonstrated high affinity and pharmacological potential targeting these genes.
conclusionsThis study unveils the link between NETs formation and OP, highlighting NCF2 as crucial players. These findings provide new insights into immune inflammation's role in bone metabolism and pave the way for targeted OP therapies.
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