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Updated: Jan 24, 2026
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Identifying a marked inflammation mediated cardiac dysfunction during the development of arthritis in
Zihao Zhou1, Zhengyue Miao2, Aishu Luo3
1Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Insights
Systemic inflammation in rheumatoid arthritis (RA) is linked to cardiovascular disease (CVD). This study shows joint inflammation in mice models causes cardiac dysfunction and inflammation in heart cells, supporting inflammation
Area of Science:
- Cardiovascular Biology
- Rheumatology
- Immunology
Background:
- Rheumatoid arthritis (RA) is associated with a higher risk of cardiovascular diseases (CVD).
- Systemic inflammation in RA plays a crucial role in the development of CVD.
- Understanding the direct impact of RA-induced inflammation on cardiac function is vital.
Purpose of the Study:
- To investigate cardiac changes during arthritis development in a collagen-induced arthritis (CIA) mouse model.
- To explore the role of inflammation in RA-associated cardiac dysfunction.
- To establish a link between joint inflammation and cardiac pathology.
Main Methods:
- Arthritis severity was assessed using clinical indices, micro-CT, and histopathology.
- Cardiac function was evaluated using transthoracic echocardiography at multiple time points.
- Gene expression of inflammatory markers and cardiac-related genes (e.g., β-MHC) was measured in isolated heart cells and cell lines exposed to serum from CIA mice or RA patients.
Main Results:
- CIA mice exhibited significantly reduced cardiac function, indicated by decreased ejection fraction (EF) and fractional shortening (FS).
- Pathological analysis revealed increased inflammatory cell infiltration and fibrosis in ventricular tissues.
- Elevated expression of inflammatory cytokines (TNF-α, IL-6, IL-17) and MMP3 was observed in cardiomyocytes and cardiac fibroblasts; β-MHC expression increased in H9c2 cells treated with CIA/RA sera.
Conclusions:
- Joint inflammation in RA is directly associated with cardiac dysfunction.
- Inflammation promotes cardiac infiltration and inflammatory cytokine production in heart cells during CIA.
- This study provides direct evidence that inflammation contributes to cardiac disease development in RA patients.
Objectives:
Systemic inflammation is very closely linked to the increased risk of cardiovascular diseases (CVD) in rheumatoid arthritis (RA). We investigated the cardiac changes during the development of arthritis in collagen-induced arthritis (CIA) mice to explore the potential role of inflammation on cardiac dysfunction in RA.
Methods:
Arthritis severity was evaluated using clinical indices, micro-computed tomography and histopathology. Cardiac function was determined by transthoracic echocardiography at weeks 5, 7, 9 and 11 after immunisation in mice. At week 7 (day 50), mice joints and hearts were removed for pathological study, and cardiomyocytes and cardiac fibroblasts were isolated using Langendorff perfusion method ex vivo to measure the expression of inflammatory and cardiac-related genes by real time PCR. The expression of key molecule in cardiac dysfunction (β-MHC) was also tested in H9c2 cardiomyocyte treated with sera derived from CIA mice or RA patients.
Results:
At day 50 after immunisation, cardiac function in CIA mice was prominently reduced as evidenced by decreased ejection fraction (EF) and fractional shortening (FS), increased left ventricular end-systolic volume (LVESV) and internal systolic diameter (LVIDs). Accordingly, enhanced inflammatory cell infiltration and fibrosis were identified in ventricular tissues pathologically, and increased inflammatory gene expression including TNF-α, IL-6, IL-17 and MMP3 was detected in isolated ventricular cardiomyocytes and cardiac fibroblasts from CIA mice. Furthermore, H9c2 cells treated with sera from CIA mice or RA patients exhibited high levels of β-MHC.
Conclusions:
Joint inflammation is associated with an obvious cardiac dysfunction and enhanced inflammation infiltration and inflammatory cytokine production in cardiomyocytes and cardiac fibroblasts during CIA development. Our data provide the direct evidence that inflammation contributes to the development of cardiac diseases in RA patients.
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