Evidence mapPaperPMID 40544171Full record

ReviewNature reviews. Cardiology2025

Immunometabolism in heart failure.

Ioanna Andreadou, Alessandra Ghigo, Panagiota-Efstathia Nikolaou, Filip K Swirski, James T Thackeray, Gerd Heusch, Gemma Vilahur

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed.

  1. Chemical Bond-Orchestrated Energy Depletion to Augment Lung Cancer Chemo-Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  16. Coenzyme QInternational journal of molecular sciences · 2026
    Article
  17. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Ioanna Andreadou *Laboratory of Pharmacology, School of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece.
Alessandra Ghigo *Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center 'Guido Tarone', University of Torino, Torino, Italy.ORCID 0000-0002-1193-5296
Panagiota-Efstathia NikolaouLaboratory of Pharmacology, School of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece.ORCID 0000-0002-7777-6726
Filip K SwirskiCardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.ORCID 0000-0002-3163-9152
James T ThackerayTranslational Cardiovascular Molecular Imaging, Department of Nuclear Medicine, Hannover Medical School, Hannover, Germany.
Gerd HeuschCardioprotection Unit, Institute for Pathophysiology, West German Heart and Vascular Center, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0001-7078-4160
Gemma VilahurSant Pau Research Institute (IR SANT PAU), Barcelona, Spain. gvilahur@santpau.cat.ORCID 0000-0002-2828-8873

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction between inflammation and metabolism (immunometabolism) is a crucial factor in the pathophysiology of heart failure, whether the cardiac failure originates from ischaemic injury or systemic metabolic disorders, and whether it is associated with reduced or preserved ejection fraction. Ischaemia, metabolic stress and comorbidity-driven systemic inflammation attract innate and adaptive immune cells to the myocardium and induce their polarization towards pro-inflammatory or anti-inflammatory phenotypes through cell-intrinsic metabolic shifts involving oxidative phosphorylation and anaerobic glycolysis. These infiltrating immune cells modulate cardiac and systemic metabolism. The bidirectional metabolic crosstalk between immune cells and parenchymal and stromal cardiac cells contributes to adverse cardiac remodelling. In turn, ischaemic injury and deregulated metabolism stimulate bone marrow and extramedullary myelopoiesis, which increases immune cell recruitment and perpetuates a non-resolving chronic inflammatory state. Pharmacological interventions targeting metabolism have shown promise for improving outcomes in patients with heart failure, but immunomodulatory approaches face multiple challenges. Understanding the complex metabolic pathways and cell-cell interactions that regulate immunometabolism in heart failure is essential to identify new therapies that shift the balance from maladaptive to cardioprotective immune responses. In this Review, we provide a comprehensive overview of the intricate cellular and molecular mechanisms that govern immunometabolism in heart failure and discuss potential approaches to non-invasively monitor and treat patients with heart failure.

Indexed as

Energy MetabolismHeart FailureInflammationMyocardiumAnimalsHumans

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.