Cells, Volume 8, Issue 12 (December 2019) – 189 articles
Cover Story (view full-size image): Rheumatoid arthritis (RA) is a chronic inflammatory disease that causes progressive joint destruction over time. RA is characterized by extensive synovitis, cartilage erosion, and bone destruction by excessive immune and inflammatory responses. Synovial cells and immune cells produce inflammatory cytokines, such as IL-1, IL-6, and TNFα, and matrix metalloproteases (MMPs). Since NF-ĸB is a transcription factor that regulates the expression of inflammatory cytokines, including TNF-α and IL-6, and serves as a mediator for RANK signaling, selective inhibition of the classical NF-ĸB pathway appears to be a target for bone destruction of RA. NF-ĸB inhibitors, such as decoy oligonucleotides, NEMO-biding domain (NBD) peptide, TAT-IĸBα-super repressor, or IKKβ inhibitor, suppress bone destruction by suppressing local inflammation and RANK signaling. View this paper.
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