Subclinical atherosclerosis in rheumatoid arthritis is driven by MicroRNA polymorphisms and NETosis
Authors' conclusion
miR-SNPs rs2431697 and rs3746444 are associated with subclinical atherosclerosis in RA and, in the case of rs2431697, preliminary results suggest that NETosis could be an underlying mechanism.
Study context
- Population
- Rheumatoid arthritis (RA) patients and healthy controlsCarotid intima-media thickness (CIMT) in 65 RA, 75 controls
- Participants
- 620 vs 359
- Comparison
- RA vs healthy controls; miR-SNP genotypes and pathological CIMT (pCIMT)
- RAn = 620
- Controlsn = 359reference
- Outcome
- Association of miR-SNPs (rs2431697, rs3746444, rs11614913) with subclinical atherosclerosis (pCIMT) in RA, and mediation by NETosis
Methodological detailslogistic regression adjusted for RA status and cardiovascular risk factors
- Logistic regression adjusted for RA status and cardiovascular risk factors
Main finding
As reported in the abstract
Pathological CIMT (pCIMT)
P < 0.001
Observational data: associations, not effects.
Further findings
RA susceptibility
- rs11614913 C allele associated with RA susceptibility
NETosis marker citH3-DNA
- rs2431697 T allele associated with increased citH3-DNA levels, suggesting enhanced NETosis
Original publication
Subclinical atherosclerosis in rheumatoid arthritis is driven by MicroRNA polymorphisms and NETosis. Arthritis Res Ther. Published 9 February 2026. doi:10.
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