Psoriatic Arthritis: Pathogenesis and Targeted Therapies
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".
Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 21103
Special Issue Editor
Interests: synovial immunopathology; biomarkers (clinical, serum and synovial tissue) diagnostic and prognostics - response to biological therapies); cytokines in biofluids and synovial tissue; lipidomics comparing psoriatic arthritis and rheumatoid arthritis; epigenomics (DNA methylation) related with disease activity and prognosis; genomics in psoriatic arthritis and rheumatoid arthritis
Special Issue Information
Dear Colleagues,
Psoriatic arthritis (PsA) is a chronic inflammatory immune-mediated disease that usually involves the skin and several musculoskeletal sites (joint, enthesis, and axial skeleton), and can also extend to the eye (uveitis) and the bowel (bowel inflammatory disease). Furthermore, patients with PsA also show an increase in the prevalence of classical (T2 diabetes, hypertension, metabolic syndrome, obesity) and non-classical (systemic inflammation) cardiovascular risk factors, leading to a rise in morbidity and mortality.
Advances in basic and clinical research in the last two decades have improved our understanding of pathogenesis and helped the development of targeted therapies that provide better control of the disease and improve patients’ quality of life. Genomic and immunological studies in biofluids and synovial tissue of PsA patients have demonstrated two main immune-inflammatory pathways in PsA: TNFalfa and IL-23/IL-17. However, while skin has a higher expression of the IL-23/IL-17-related gene, in synovial tissue, there is higher TNFalfa-related gene expression. This discordance in cytokine expression among different tissues explains the differential therapeutic response between skin and joint to those cytokine inhibitors in PsA. Moreover, around 60% of PsA patients do not achieve significant clinical response (ACR50%) with the current targeted biological and synthetic therapies.
Therefore, addressing clinical heterogeneity and tissue pathogenesis diversity is one important step to better understand the molecular pathways resulting in different PsA endotypes. Finally, the definition of endotypes will inform therapy choice.
This Special Issue focused in “Psoriatic Arthritis: Pathogenesis and Targeted Therapies” will welcome revisions and original articles aiming to understand the link between cellular and molecular expression patterns and clinical heterogeneity, including the response to distinct targeted therapies in PsA. Some suggestions are:
- Transcriptomic, proteomic, or single-cell–RNAseq analysis of the different tissues involved in PsA to gain insights on their molecular diversity and potentially reveal new targets;
- Cytokine expression patterns (at the protein and mRNA level) in biofluids and/or involved tissues and its association with response to therapy;
- Epigenetic (DNA methylation, mirRNA), lipidomics, and other -omic techniques looking at differences of translational/clinical relevance between PsA and rheumatoid arthritis or undifferentiated arthritis;
- Other suggested articles related to the topic.
Dr. Juan D. Cañete
Guest Editor
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Keywords
- psoriatic arthritis
- targeted therapies
- rheumatoid arthritis
- epigenetic
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