Key result
Aberrant SNPs and alternative splicing in over 100 immune loci linked to rheumatoid arthritis induction.
Why the study?
Genetic factors account for substantial rheumatoid arthritis risk, and aberrant single nucleotide polymorphisms and alternative splicing mechanisms in associated loci represent potential therapeutic targets.
Aberrant SNPs and alternative splicing mechanisms in immune regulatory genes are potential therapeutic targets for Rheumatoid Arthritis.
May identify RA therapeutic targets; leaves open validation in prospective trials before clinical adoption.
Advances in genomics and proteomics aid the identification of genes associated with various diseases. Genome-Wide Association Studies (GWAS) have identified multiple loci as risk alleles for susceptibility to Rheumatoid Arthritis (RA). A bisection of RA risk can be attributed to genetic factors. Over 100 associated genetic loci that encompass immune regulatory factors have been found to be linked with RA. Aberrant Single Nucleotide Polymorphisms (SNPs) and alternative splicing mechanisms in such loci induce RA. These aberrations are viewed as potential therapeutic targets due to their association with a multitude of diseases. This review presents a few imperious genes whose alterations can cause severe bone deformities culminating in RA.
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Aravilli et al. (2020) conducted a review in Rheumatoid Arthritis. Alternative splicing and Single Nucleotide Polymorphisms was evaluated. Aberrant single nucleotide polymorphisms and alternative splicing mechanisms in over 100 genetic loci encompassing immune regulatory factors are linked to the induction of rheumatoid arthritis.
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