NDLI: Impact of Posttranslational Modification in Pathogenesis of Rheumatoid Arthritis: Focusing on Citrullination, Carbamylation, and Acetylation

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Impact of Posttranslational Modification in Pathogenesis of Rheumatoid Arthritis: Focusing on Citrullination, Carbamylation, and Acetylation

Content Provider	MDPI
Author	Kwon, Eui-Jong Ju, Ji Hyeon
Copyright Year	2021
Description	Rheumatoid arthritis (RA) is caused by prolonged periodic interactions between genetic, environmental, and immunologic factors. Posttranslational modifications (PTMs) such as citrullination, carbamylation, and acetylation are correlated with the pathogenesis of RA. PTM and cell death mechanisms such as apoptosis, autophagy, NETosis, leukotoxic hypercitrullination (LTH), and necrosis are related to each other and induce autoantigenicity. Certain microbial infections, such as those caused by Porphyromonasgingivalis, Aggregatibacter actinomycetemcomitans, and Prevotella copri, can induce autoantigens in RA. Anti-modified protein antibodies (AMPA) containing anti-citrullinated protein/peptide antibodies (ACPAs), anti-carbamylated protein (anti-CarP) antibodies, and anti-acetylated protein antibodies (AAPAs) play a role in pathogenesis as well as in prediction, diagnosis, and prognosis. Interestingly, smoking is correlated with both PTMs and AMPAs in the development of RA. However, there is lack of evidence that smoking induces the generation of AMPAs.
Starting Page	10576
e-ISSN	14220067
DOI	10.3390/ijms221910576
Journal	International Journal of Molecular Sciences
Issue Number	19
Volume Number	22
Language	English
Publisher	MDPI
Publisher Date	2021-09-30
Access Restriction	Open
Subject Keyword	International Journal of Molecular Sciences Rheumatology Rheumatoid Arthritis Pathogenesis Posttranslational Modification (ptm) Citrullination Carbamylation Acetylation Anti-modified Protein Antibodies (ampas) Anti-citrullinated Protein/peptide Antibodies (acpas) Anti-carbamylated Protein (anti-carp) Antibodies Anti-acetylated Protein Antibodies (aapas)
Content Type	Text
Resource Type	Article

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