Related Experiment Videos
Gene polymorphism and serum level of RANKL among patients with rheumatoid arthritis: a systematic review and
Pouria Salajegheh1, Amirali Salajegheh2, Farzaneh Yazdi3
1Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran. salajegheh.poorya@gmail.com.
Receptor activator of nuclear factor-κB ligand (RANKL) is a key mediator linking inflammation to osteoclast activation and bone erosion in rheumatoid arthritis (RA). Evidence on circulating RANKL levels and RANKL (TNFSF11) polymorphisms in RA has been inconsistent. Web of Science, Scopus, and PubMed were searched from inception to December 2025 for clinical studies comparing patients with RA and healthy controls and reporting either serum/plasma RANKL concentrations and/or RANKL genotype/allele distributions. Mean differences (MD) were pooled for circulating RANKL, and odds ratios (OR) were pooled for polymorphisms under allelic, dominant, and recessive models. Ten studies (908 RA; 525 controls) were included for serum RANKL. Serum RANKL was higher in RA than controls (pooled MD 8.16, 95% CI 3.90-12.41). For genetic analyses, three SNPs were eligible for pooling. rs9533156 showed a significant association with RA in the allelic (C vs T: OR 0.82, 95% CI 0.70-0.97) and dominant models (CC+CT vs TT: OR 0.77, 95% CI 0.61-0.98). rs2277438 showed a borderline allelic association (OR 1.21, 95% CI 1.00-1.45) and model-dependent results for the recessive contrast with heterogeneity. RA is associated with increased circulating RANKL, while genetic associations appear SNP-specific, with the most consistent evidence observed for rs9533156. Larger, multi-ethnic studies with standardized biomarker measurements are needed.
Receptor activator of nuclear factor-κB ligand (RANKL) is a key mediator linking inflammation to osteoclast activation and bone erosion in rheumatoid arthritis (RA). Evidence on circulating RANKL levels and RANKL (TNFSF11) polymorphisms in RA has been inconsistent. Web of Science, Scopus, and PubMed were searched from inception to December 2025 for clinical studies comparing patients with RA and healthy controls and reporting either serum/plasma RANKL concentrations and/or RANKL genotype/allele distributions. Mean differences (MD) were pooled for circulating RANKL, and odds ratios (OR) were pooled for polymorphisms under allelic, dominant, and recessive models. Ten studies (908 RA; 525 controls) were included for serum RANKL. Serum RANKL was higher in RA than controls (pooled MD 8.16, 95% CI 3.90-12.41). For genetic analyses, three SNPs were eligible for pooling. rs9533156 showed a significant association with RA in the allelic (C vs T: OR 0.82, 95% CI 0.70-0.97) and dominant models (CC+CT vs TT: OR 0.77, 95% CI 0.61-0.98). rs2277438 showed a borderline allelic association (OR 1.21, 95% CI 1.00-1.45) and model-dependent results for the recessive contrast with heterogeneity. RA is associated with increased circulating RANKL, while genetic associations appear SNP-specific, with the most consistent evidence observed for rs9533156. Larger, multi-ethnic studies with standardized biomarker measurements are needed.
Related Concept Videos
01:20The JAK-STAT Signaling Pathway
01:11Genome-wide Association Studies-GWAS
GWAS does not require the identification of the target gene involved in...