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Updated: Aug 24, 2025

Isolation of Functional Cardiac Immune Cells
Published on: December 5, 2011
[Pro-inflammatory cytokines in chronic cardiac failure: state of problem]
A A Korotaeva1, E V Samoilova1, D R Mindzaev1
1National Medical Research Center for Cardiology.
Insights
Systemic inflammation, marked by pro-inflammatory cytokines like interleukin-6, plays a role in chronic heart failure (CHF) progression. Targeting these cytokines for CHF therapy presents challenges, necessitating further research into specific inflammatory pathways.
Area of Science:
- Cardiology
- Immunology
- Biomedical Science
Context:
- Systemic inflammation and pro-inflammatory cytokines are hallmarks of chronic heart failure (CHF).
- Elevated cytokine levels in CHF patients correlate with adverse clinical outcomes.
- Distinct inflammatory profiles exist between CHF with preserved ejection fraction (HFpEF) and CHF with reduced ejection fraction (HFrEF).
Purpose:
- To review the role of pro-inflammatory cytokines in the pathophysiology of CHF.
- To highlight the activation of interleukin-6 (IL-6) and its impact on CHF.
- To examine the influence of comorbidities on systemic inflammation in CHF.
Summary:
- Pro-inflammatory cytokines contribute to CHF development, with IL-6 playing a significant role.
- Comorbidities exacerbate systemic inflammation in CHF patients.
- Clinical trials of anti-cytokine therapies in CHF have faced challenges in controlling inflammation.
Impact:
- Identifying specific pro-inflammatory pathways in CHF pathogenesis is crucial.
- Targeting these pathways offers a prospective therapeutic strategy for CHF.
- Further research is needed to refine anti-cytokine therapies for improved CHF management.
Abstract:
Systemic inflammation is characterized by the induction of pro-inflammatory cytokines, the increased level of which in the blood of patients with chronic heart failure (CHF) correlates with unfavorable clinical outcomes. However, it is unclear whether pro-inflammatory cytokines are the cause or the consequence of the disease progression. CHF with preserved ejection fraction and CHF with reduced ejection fraction demonstrate different inflammatory features, which suggests different degrees of pro-inflammatory pathway activation. The review deals with participation of pro-inflammatory cytokines in pathophysiological processes of CHF development, emphasizing the role of interleukin-6 activation and the effects of accompanying diseases on the course of systemic inflammation. The search for new approaches to prevention and therapy of CHF remains actual. The review presents the results of clinical trials of targeted anti-cytokine therapy which have revealed difficulties in controlling inflammation under the conditions of CHF. Identification of specific pro-inflammatory pathways in CHF pathogenesis will allow one to control inflammatory cascades, thus providing a prospective therapeutic strategy.
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