A defined cytokine regimen drives durable cardioprotection and fibrosis reversal in experimental heart failure
Clicks: 2
ID: 323343
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
0.3
/100
2 views
1 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #187 of 282 articles by views in European heart journal supplements : journal of the European Society of Cardiology
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 282 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Abstract Background Heart failure remains a leading cause of mortality worldwide, and current therapies largely provide symptomatic benefit without reversing fibrosis or cardiac dysfunction. Tumour-associated immune signalling has been shown to exert cardioprotective effects; however, the mechanisms required for sustained cardiac recovery remain unknown. Purpose To define the cytokine requirements necessary to achieve durable cardioprotection and fibrosis suppression in experimental heart failure. Methods Murine models of heart failure, including dystrophin-deficient cardiomyopathy and pressure overload–induced disease, were treated with immune-derived cytokines identified from tumour-associated serum. Cardiac function was assessed by echocardiography, and myocardial fibrosis was quantified histologically. Single versus repeated cytokine administration strategies were compared to evaluate durability of response. Results Interferon-gamma and tumour necrosis factor-alpha transiently improved ventricular function and reduced myocardial fibrosis but failed to confer sustained benefit upon repeated dosing. Interleukin-13 similarly induced short-lived functional improvement when administered alone. In contrast, repeated co-administration of interferon-gamma, tumour necrosis factor-alpha, and interleukin-13 produced a sustained increase in ventricular contractility and persistent suppression of myocardial fibrosis. This defined cytokine triad fully recapitulated the durable cardioprotective phenotype observed with tumour-derived serum. Conclusion Durable cardiac recovery requires coordinated activation of complementary immune cytokine pathways. A defined cytokine-based regimen comprising interferon-gamma, tumour necrosis factor-alpha, and interleukin-13 induces sustained cardioprotection and fibrosis reversal in heart failure models, providing a translational framework for immune-modulatory therapies in acquired and muscular dystrophy–associated cardiomyopathies.
| Reference Key |
openalex_W7172346419
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | L Achlaug, L Awwad, I Langier Goncalves, S Aviram, A Glasner, A Aronheim |
| Journal | European heart journal supplements : journal of the European Society of Cardiology |
| Year | 2026 |
| DOI |
10.1093/eurheartjsupp/suag097.002
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.