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Post Translational Modification and Its Pathologic Association in Rheumatoid Arthritis: A Brief Perspective
Vishnupreetha Vasudevan1, Prachi Agnihotri1, Sagarika Biswas1
1Council of Industrial Research (CSIR)-Institute of Genomics and Integrative Biology, Mall Road, Delhi University Campus, Delhi, 110007, India.
Current Protein & Peptide Science
|February 16, 2021
Summary
Post-translational modifications (PTMs) can trigger autoimmunity, leading to diseases like rheumatoid arthritis (RA). This review explores how altered PTMs contribute to RA pathogenesis and autoantibody generation, emphasizing early diagnosis.
Area of Science:
- Biochemistry
- Immunology
- Rheumatology
Background:
- Post-translational modifications (PTMs) regulate protein function but can cause autoimmunity when dysregulated.
- Rheumatoid arthritis (RA) is a chronic autoimmune disease impacting joints and potentially other organs, necessitating early diagnosis.
- Current RA biomarkers include Rheumatoid Factor (RF) and anti-citrullinated cyclic peptide (Anti-CCP).
Purpose of the Study:
- To review the role of various PTMs in the pathogenesis of rheumatoid arthritis.
- To elucidate changes in the form, nature, and function of PTMs in RA.
- To provide an updated overview of PTMs in RA, focusing on their contribution to autoantibody generation.
Main Methods:
- Literature review of PTMs in rheumatoid arthritis.
- Analysis of PTMs beyond citrullination involved in autoantibody generation.
- Focus on PTMs' role in RA pathogenesis.
Main Results:
- Dysregulated PTMs, including carbamylation, glycosylation, and acetylation, contribute to RA autoimmunity.
- Multiple PTMs are implicated in the generation of autoantibodies relevant to RA.
- Understanding PTM alterations is crucial for RA diagnosis and management.
Conclusions:
- Altered PTMs are integral to rheumatoid arthritis pathogenesis.
- PTMs beyond citrullination play significant roles in RA autoantibody production.
- Further research into PTMs can improve early RA diagnosis and treatment strategies.
Keywords:
Post-translational modificationRheumatoid arthritisanticitrullinatedncyclic
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