Evidence map›Paper›PMID 33053859›Full record

ReviewJournal of clinical medicine2020

Complexity of TNF-α Signaling in Heart Disease.

Filip Rolski, Przemysław Błyszczuk

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 2 pooled it
12.9field-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

95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 167 citations in OpenAlex.

  1. Immunology of heart failure with preserved ejection fraction.Expert review of clinical immunology · 2025
    Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
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  10. Long-term artificial sweetener exposure increases the risk of atherosclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  11. Article
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  13. Article
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  15. Article
  16. Review
  17. Inulin may inhibit ADAM17 to delay atherosclerosis.Open medicine (Warsaw, Poland) · 2026
    Article
  18. Review
  19. Article
  20. Article

35 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.

Filip RolskiDepartment of Clinical Immunology, Jagiellonian University Medical College, 30-663 Cracow, Poland.
Przemysław BłyszczukDepartment of Clinical Immunology, Jagiellonian University Medical College, 30-663 Cracow, Poland.ORCID 0000-0003-2521-3232
Jagiellonian University · PL

Funding

National Science Centre (Poland) 2016/21/B/NZ5/01397
6 · The paper itself

Abstract

Heart disease is a leading cause of death with unmet clinical needs for targeted treatment options. Tumor necrosis factor alpha (TNF-α) represents a master pro-inflammatory cytokine that plays an important role in many immunopathogenic processes. Anti-TNF-α therapy is widely used in treating autoimmune inflammatory disorders, but in case of patients with heart disease, this treatment was unsuccessful or even harmful. The underlying reasons remain elusive until today. This review summarizes the effects of anti-TNF-α treatment in patients with and without heart disease and describes the involvement of TNF-α signaling in a number of animal models of cardiovascular diseases. We specifically focused on the role of TNF-α in specific cardiovascular conditions and in defined cardiac cell types. Although some mechanisms, mainly in disease development, are quite well known, a comprehensive understanding of TNF-α signaling in the failing heart is still incomplete. Published data identify pathogenic and cardioprotective mechanisms of TNF-α in the affected heart and highlight the differential role of two TNF-α receptors pointing to the complexity of the TNF-α signaling. In the light of these findings, it seems that targeting the TNF-α pathway in heart disease may show therapeutic benefits, but this approach must be more specific and selectively block pathogenic mechanisms. To this aim, more research is needed to better understand the molecular mechanisms of TNF-α signaling in the failing heart.

Indexed as

cardiac fibrosiscardiovascular diseaseheartinflammationTNFR1TNFR2TNF-α

Identifiers

PMID33053859
PMCPMC7601316
OpenAlexW3092363281

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.