Evidence map›Paper›PMID 32053869›Full record

ReviewCells2020

Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in Cardiovascular Diseases: Progress and Challenges.

Nerea Méndez-Barbero, Carmen Gutiérrez-Muñoz, Rafael Blázquez-Serra, Jose L Martín-Ventura, Luis M Blanco-Colio

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Expression and significance ofBiomarkers in medicine · 2025
    Article
  11. Article
  12. [Two-sample Mendelian randomization analysis for the causal relationship between 91 circulating inflammatory proteins and liver cirrhosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review
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

5 authors at 1 institution in 1 country.

Nerea Méndez-BarberoVascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital, Av. Reyes Católicos 2, 28040 Madrid, Spain.
Carmen Gutiérrez-MuñozVascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital, Av. Reyes Católicos 2, 28040 Madrid, Spain.
Rafael Blázquez-SerraVascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital, Av. Reyes Católicos 2, 28040 Madrid, Spain.
Jose L Martín-VenturaVascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital, Av. Reyes Católicos 2, 28040 Madrid, Spain.
Luis M Blanco-ColioVascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital, Av. Reyes Católicos 2, 28040 Madrid, Spain.
Centro de Investigación en Red en Enfermedades Cardiovasculares · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases (CVD) are the leading cause of mortality in Western countries. CVD include several pathologies, such as coronary artery disease, stroke, peripheral artery disease, and aortic aneurysm, among others. All of them are characterized by a pathological vascular remodeling in which inflammation plays a key role. Interaction between different members of the tumor necrosis factor superfamily and their cognate receptors induce several biological actions that may participate in CVD. The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), are abundantly expressed during pathological cardiovascular remodeling. The TWEAK/Fn14 axis controls a variety of cellular functions, such as proliferation, differentiation, and apoptosis, and has several biological functions, such as inflammation and fibrosis that are linked to CVD. It has been demonstrated that persistent TWEAK/Fn14 activation is involved in both vessel and heart remodeling associated with acute and chronic CVD. In this review, we summarized the role of the TWEAK/Fn14 axis during pathological cardiovascular remodeling, highlighting the cellular components and the signaling pathways that are involved in these processes.

Indexed as

ApoptosisCardiovascular DiseasesCytokine TWEAKHeart Disease Risk FactorsHumansInflammationSignal TransductionTWEAK ReceptorVentricular RemodelingCytokine TWEAKTNFRSF12A protein, humanTNFSF12 protein, humanTWEAK ReceptorFn14heart failurestrokeTWEAKvascular remodeling

Identifiers

PMID32053869
PMCPMC7072601
OpenAlexW3004523546

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.