Abstract
Rheumatoid arthritis (RA) is a systemic poly-articular chronic autoimmune joint disease that mainly damages the hands and feet, which affects 0.5% to 1.0% of the population worldwide. With the sustained development of disease-modifying antirheumatic drugs (DMARDs), significant success has been achieved for preventing and relieving disease activity in RA patients. Unfortunately, some patients still show limited response to DMARDs, which puts forward new requirements for special targets and novel therapies. Understanding the pathogenetic roles of the various molecules in RA could facilitate discovery of potential therapeutic targets and approaches. In this review, both existing and emerging targets, including the proteins, small molecular metabolites, and epigenetic regulators related to RA, are discussed, with a focus on the mechanisms that result in inflammation and the development of new drugs for blocking the various modulators in RA.
Highlights
Rheumatoid arthritis (RA) is classified as a systemic poly-articular chronic autoimmune joint disease that primarily affects hands and feet
In RA patients, an alteration of DNA methylome signature in peripheral blood mononuclear (PBMC) and a reduction of 5-mC amounts in synovial tissues were observed, the alteration of fibroblast-like synoviocytes (FLS) gene expression, including chitinase-3-like protein 1 (CHI3L1), caspase 1 (CASP1), STAT3, mitogen-activated protein kinase kinase kinase 5 (MAP3K5), familial Mediterranean fever (MEFV), and wnt1-inducible signaling protein 3 (WISP3), is caused by differentially methylated genes leading to the pathogenesis of RA [293]
RA is an autoimmune disease with complex etiology
Summary
Rheumatoid arthritis (RA) is classified as a systemic poly-articular chronic autoimmune joint disease that primarily affects hands and feet.
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