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Updated: Jun 15, 2026
Echocardiographic Assessment of the Right Heart in Mice
Published on: November 27, 2013
Circulating cytokine levels in mice with heart failure are etiology dependent
Maria Vistnes1, Anne Waehre, Ståle Nygård
1Institute for Experimental Medical Research, Oslo University Hospital Ullevål, and Center for Heart Failure Research, University of Oslo, Kirkeveien 166, N-0407 Oslo, Norway. r.m.vistnes@studmed.uio.no
Insights
Cytokine levels in heart failure (HF) vary by cause. Increased right ventricular afterload, leading to systemic congestion, appears to drive elevated cytokine levels in HF mouse models.
Area of Science:
- Cardiovascular Research
- Immunology
- Biomarker Discovery
Background:
- Altered circulating cytokine levels are observed in various heart diseases.
- Cytokines are potential biomarkers and therapeutic targets for heart conditions.
- Understanding etiology-dependent cytokine changes is crucial for clinical applications.
Purpose of the Study:
- To investigate if circulating cytokine level alterations depend on the specific cause of myocardial hypertrophy and heart failure (HF).
Main Methods:
- Quantified serum levels of 25 cytokines using Luminex and/or ELISA.
- Utilized four distinct murine models of heart disease: ascending aorta banding (AB), pulmonary artery banding (PB), myocardial infarction (MI), and a SERCA2 knockout (SERCA2KO) cardiomyopathy model.
Main Results:
- No significant cytokine increase was noted in AB mice with hypertrophy.
- Only interleukin-18 (IL-18) increased post-myocardial infarction (MI).
- SERCA2KO and PB models (increased right ventricular afterload) showed elevated levels of multiple cytokines, including IL-1alpha, IL-6, and G-CSF, suggesting a link to systemic congestion.
Conclusions:
- Serum cytokine profiles in heart failure (HF) are etiology-dependent.
- Elevated cytokines in models with increased right ventricular afterload indicate systemic congestion as a primary driver.
- Findings emphasize the need to consider disease cause when using cytokines as HF biomarkers or therapeutic targets.
Objectives:
The aim of this study was to examine whether alterations in circulating cytokine levels are dependent on the etiology of myocardial hypertrophy and heart failure (HF).
Background:
Several heart diseases are associated with altered levels of circulating cytokines. Cytokines are regarded as possible therapeutic targets or biomarkers, but such approaches are currently not in clinical use. If alterations in circulating cytokines are etiology dependent, this should be taken into consideration when using cytokines as disease markers and therapeutic targets.
Methods:
The serum levels of 25 cytokines were quantified with Luminex and/or ELISA in four murine models of heart disease: banding of the ascending aorta (AB) or the pulmonary artery (PB), myocardial infarction (MI), and a cardiomyopathy model with inducible cardiomyocyte-specific knockout of the sarco(endo)plasmatic reticulum Ca2+-ATPase (SERCA2KO).
Results:
No increase in circulating cytokine levels were found in mice 1 wk after AB, although substantial myocardial hypertrophy was present. After 1 wk of MI, only interleukin (IL)-18 was increased. In the SERCA2KO mice with HF, circulating levels of IL-1alpha, IL-2, IL-3, IL-6, IL-9, IL-10, IL-12p40, eotaxin, granulocyte-colony stimulating factor (G-CSF), interferon-gamma, monocyte chemoattractant protein-1, macrophage inflammatory protein-1beta were increased, and in mice with PB, IL-1alpha, IL-6, G-CSF, and monokine induced by gamma-interferon showed elevated levels.
Conclusions:
Serum levels of cytokines in mice with HF vary depending on the etiology. Increased serum levels of several cytokines were found in models with increased right ventricular afterload, suggesting that the cytokine responses result primarily from systemic congestion.
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