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Rheumatic Heart Disease III: Medical Management01:21

Rheumatic Heart Disease III: Medical Management

Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Preliminary Study on Acupuncture Combined with Grain-sized Moxibustion for Treating Rheumatoid Arthritis with Finger Joint Pain
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The Relationship Between CCN3 and Rheumatoid Arthritis and Its Potential Therapeutic Value.

Ye Yuan1,2,3, Hui Yin1, Mengya Jiao2,3,4

  • 1Department of Microbiology and Immunology, School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China, gdpu.edu.cn.

Journal of Immunology Research
|July 6, 2026
PubMed
Summary

Cellular communication network factor 3 (CCN3) is elevated in rheumatoid arthritis (RA) and drives disease processes like inflammation and joint damage. Targeting CCN3 shows promise for new RA therapies.

Keywords:
CCN3immune regulationinflammationjoint destructionrheumatoid arthritis

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Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease causing synovial inflammation and joint destruction.
  • Current disease-modifying antirheumatic drugs (DMARDs) have limitations in efficacy and safety.
  • Novel therapeutic targets are needed to address unmet clinical needs in RA management.

Purpose of the Study:

  • To review the role of Cellular Communication Network factor 3 (CCN3) in rheumatoid arthritis.
  • To examine CCN3's expression, functions, and signaling pathways in RA.
  • To explore CCN3 as a potential therapeutic target for RA.

Main Methods:

  • Comprehensive literature review of studies on CCN3 in RA.
  • Analysis of CCN3 expression patterns in normal and RA synovium and circulation.
  • Examination of CCN3's functional effects on inflammatory cells, synoviocytes, and joint tissues.
  • Investigation of CCN3's interactions with key signaling pathways implicated in RA pathogenesis.

Main Results:

  • CCN3 expression is low in normal synovium but significantly elevated in RA synovium and circulation.
  • Elevated CCN3 levels correlate with RA disease activity, anti-CCP antibody titers, and IL-6 levels.
  • CCN3 influences inflammatory cell recruitment, fibroblast-like synoviocyte activation and senescence, ECM remodeling, cartilage degradation, and osteoclastogenesis.
  • CCN3 interacts with multiple RA-relevant signaling pathways including NF-κB, Wnt/β-catenin, BMP/Smad, PI3K/Akt/mTOR, IL-6/JAK/STAT, Notch, and MAPK.

Conclusions:

  • CCN3 plays a significant role in the pathogenesis of rheumatoid arthritis.
  • CCN3's multifaceted involvement in inflammation, joint destruction, and signaling pathways highlights its therapeutic potential.
  • Targeting CCN3 represents a promising strategy for developing novel RA treatments in preclinical research.