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From Pathogenesis to Treatment—New Perspectives in Rheumatology 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 2254

Special Issue Editors


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Guest Editor
1. Department of Rheumatology and Physiotherapy, “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania
2. I Rheumatology Clinic, Clinical Rehabilitation Hospital, Iasi, Romania
Interests: immune inflammatory rheumatic diseases; cytokines; biological therapy; biomarkers; autoantibodies; genetic predisposition; therapeutic targets; immune response
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Center for Rheumatic Diseases, University of Medicine and Pharmacy, Bucharest, Romania
Interests: rheumatoid arthritis; early arthritis; gout; disease registries
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent research has focused on the identification and characterization of the molecular pathways involved in chronic diseases in order to develop novel and effective treatment strategies. There is a growing body of evidence regarding the pathogenesis of immune-inflammatory rheumatic conditions, leading to significant advancements in therapeutic management. From biologicals targeting various pathogenic pathways to the more recent introduction of JAK inhibitors, there is a currently expanding array of treatment options for patients with inflammatory rheumatic diseases that are supported by robust scientific evidence. Moreover, the analysis of certain gene signatures and molecular profiles may prove useful in predicting the response to remissive treatment in rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, as well as other rheumatic diseases. Further research in this field is of utmost importance, as it may lead to an improvement in therapy choices.

Osteoarthritis is by far the most prevalent rheumatic condition, yet no pathogenic treatment is currently available. In this respect, studies related to the efficacy of potential therapeutic agents that target cartilage degradation, bone remodeling, and synovial inflammation have reported conflicting results. There is a currently unmet need for novel therapeutic options in osteoarthritis beyond symptomatic treatment.

In the present Special Issue, we aim to collect recent knowledge of the intricate pathogenic mechanisms of rheumatic conditions and their relationship with therapeutic management (novel treatment options, identification of new therapeutic targets, response to remissive treatment). Original research articles as well as reviews are welcome.

More published papers could be found in the closed Special Issue: From Pathogenesis to Treatment—New Perspectives in Rheumatology.

Dr. Elena Rezus
Dr. Catalin Codreanu
Guest Editors

Manuscript Submission Information

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Published Papers (2 papers)

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Review

15 pages, 651 KiB  
Review
Autoimmune Liver Diseases and Rheumatoid Arthritis—Is There an Etiopathogenic Link?
by Ioana Ruxandra Mihai, Ciprian Rezus, Maria Alexandra Burlui, Anca Cardoneanu, Luana Andreea Macovei, Patricia Richter, Ioana Bratoiu and Elena Rezus
Int. J. Mol. Sci. 2024, 25(7), 3848; https://doi.org/10.3390/ijms25073848 - 29 Mar 2024
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Abstract
Rheumatoid arthritis (RA) is a systemic immune-mediated disease that, in addition to the articular involvement, can have extra-articular manifestations. Even though liver damage in RA is not very common, associated autoimmune liver diseases (AILDs) may occur. The most common AILD associated with RA [...] Read more.
Rheumatoid arthritis (RA) is a systemic immune-mediated disease that, in addition to the articular involvement, can have extra-articular manifestations. Even though liver damage in RA is not very common, associated autoimmune liver diseases (AILDs) may occur. The most common AILD associated with RA is primary biliary cirrhosis (PBC), followed by autoimmune hepatitis (AIH) and primary sclerosing cholangitis (PSC). There are common underlying mechanisms that play a role in the emergence of autoimmunity and inflammation in both rheumatic and autoimmune liver diseases. Genetic studies have revealed the existence of several common disease-associated genes shared between RA and AILDs, and infectious triggers, particularly those associated with recurrent or complicated urinary tract infections, are also speculated to be potential triggers for these conditions. Moreover, these diseases share common serologic patterns characterized by the presence of specific autoantibodies and hyper-gammaglobulinemia. In this study, we focus on reviewing the association between RA and AILDs regarding the prevalence and possible etiopathogenic link. Full article
(This article belongs to the Special Issue From Pathogenesis to Treatment—New Perspectives in Rheumatology 2.0)
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17 pages, 1366 KiB  
Review
Autoimmunity and Autoinflammation: Relapsing Polychondritis and VEXAS Syndrome Challenge
by Anca Cardoneanu, Ioana Irina Rezus, Alexandra Maria Burlui, Patricia Richter, Ioana Bratoiu, Ioana Ruxandra Mihai, Luana Andreea Macovei and Elena Rezus
Int. J. Mol. Sci. 2024, 25(4), 2261; https://doi.org/10.3390/ijms25042261 - 13 Feb 2024
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Abstract
Relapsing polychondritis is a chronic autoimmune inflammatory condition characterized by recurrent episodes of inflammation at the level of cartilaginous structures and tissues rich in proteoglycans. The pathogenesis of the disease is complex and still incompletely elucidated. The data support the important role of [...] Read more.
Relapsing polychondritis is a chronic autoimmune inflammatory condition characterized by recurrent episodes of inflammation at the level of cartilaginous structures and tissues rich in proteoglycans. The pathogenesis of the disease is complex and still incompletely elucidated. The data support the important role of a particular genetic predisposition, with HLA-DR4 being considered an allele that confers a major risk of disease occurrence. Environmental factors, mechanical, chemical or infectious, act as triggers in the development of clinical manifestations, causing the degradation of proteins and the release of cryptic cartilage antigens. Both humoral and cellular immunity play essential roles in the occurrence and perpetuation of autoimmunity and inflammation. Autoantibodies anti-type II, IX and XI collagens, anti-matrilin-1 and anti-COMPs (cartilage oligomeric matrix proteins) have been highlighted in increased titers, being correlated with disease activity and considered prognostic factors. Innate immunity cells, neutrophils, monocytes, macrophages, natural killer lymphocytes and eosinophils have been found in the perichondrium and cartilage, together with activated antigen-presenting cells, C3 deposits and immunoglobulins. Also, T cells play a decisive role in the pathogenesis of the disease, with relapsing polychondritis being considered a TH1-mediated condition. Thus, increased secretions of interferon γ, interleukin (IL)-12 and IL-2 have been highlighted. The “inflammatory storm” formed by a complex network of pro-inflammatory cytokines and chemokines actively modulates the recruitment and infiltration of various cells, with cartilage being a source of antigens. Along with RP, VEXAS syndrome, another systemic autoimmune disease with genetic determinism, has an etiopathogenesis that is still incompletely known, and it involves the activation of the innate immune system through different pathways and the appearance of the cytokine storm. The clinical manifestations of VEXAS syndrome include an inflammatory phenotype often similar to that of RP, which raises diagnostic problems. The management of RP and VEXAS syndrome includes common immunosuppressive therapies whose main goal is to control systemic inflammatory manifestations. The objective of this paper is to detail the main etiopathogenetic mechanisms of a rare disease, summarizing the latest data and presenting the distinct features of these mechanisms. Full article
(This article belongs to the Special Issue From Pathogenesis to Treatment—New Perspectives in Rheumatology 2.0)
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