Evidence map›Paper›PMID 28667492›Full record

ReviewCurrent heart failure reports2017

Inflammation - Cause or Consequence of Heart Failure or Both?

Sophie Van Linthout, Carsten Tschöpe

Open access · hybridAbstract readReview
In one paragraph

Review in Current heart failure reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
274citing papers in PubMed, 5 pooled it
17.2field-weighted citation impact, top 1% of its field
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

274 citing papers in PubMed, 5 syntheses or guidelines pooled it, 447 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  5. Cancer- and cardiac-induced cachexia: same fate through different inflammatory mediators?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Pooled it
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  9. [A nomogram based on systemic inflammation markers can predict adverse outcomes in patients with heart failure].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Trial
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  13. Review
  14. Association between physical activity and long-term prognosis in older patients with Stage B heart failure.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Article
  15. Incident atrial fibrillation and pyoderma gangrenosum: long-term thromboembolic, heart failure, and mortality risk.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  16. Article
  17. Review
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  20. Cardioprotective and Antioxidant Effects of Marine-DerivedPharmaceuticals (Basel, Switzerland) · 2026
    Article

214 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sophie Van LinthoutBerlin-Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. sophie.van-linthout@charite.de.
Carsten TschöpeBerlin-Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Humboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewWith the intention to summarize the currently available evidence on the pathophysiological relevance of inflammation in heart failure, this review addresses the question whether inflammation is a cause or consequence of heart failure, or both. RECENT

findingsThis review discusses the diversity (sterile, para-inflammation, chronic inflammation) and sources of inflammation and gives an overview of how inflammation (local versus systemic) can trigger heart failure. On the other hand, the review is outlined how heart failure-associated wall stress and signals released by stressed, malfunctioning, or dead cells (DAMPs: e.g., mitochondrial DNA, ATP, S100A8, matricellular proteins) induce cardiac sterile inflammation and how heart failure provokes inflammation in various peripheral tissues in a direct (inflammatory) and indirect (hemodynamic) manner. The crosstalk between the heart and peripheral organs (bone marrow, spleen, gut, adipose tissue) is outlined and the importance of neurohormonal mechanisms including the renin angiotensin aldosteron system and the ß-adrenergic nervous system in inflammation and heart failure is discussed. Inflammation and heart failure are strongly interconnected and mutually reinforce each other. This indicates the difficulty to counteract inflammation and heart failure once this chronic vicious circle has started and points out the need to control the inflammatory process at an early stage avoiding chronic inflammation and heart failure. The diversity of inflammation further addresses the need for a tailored characterization of inflammation enabling differentiation of inflammation and subsequent target-specific strategies. It is expected that the characterization of the systemic and/or cardiac immune profile will be part of precision medicine in the future of cardiology.

Indexed as

Chronic DiseaseHeart FailureHemodynamicsHumansInflammationMyocarditisPrecision MedicineRenin-Angiotensin SystemSignal TransductionCardiosplenic axisHeart failureMonocytopoiesisPara-inflammationß-adrenergic signalingSterile inflammation

Identifiers

PMID28667492
PMCPMC5527060
OpenAlexW2730107310

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.