Evidence map›Paper›PMID 34359993›Full record

ReviewCells2021

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved.

Beatriz Delgado-Valero, Victoria Cachofeiro, Ernesto Martínez-Martínez

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Observational
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Frontiers in pharmacology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Heart Failure in Patients with Chronic Kidney Disease.Journal of clinical medicine · 2023
    Review
  14. Review
  15. Article
  16. Tetrahydrobiopterin (BHBiomedicines · 2022
    Article
  17. Review
  18. Article
  19. Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022
    Review
  20. Editorial: New Advances in Cardiorenal Syndrome.Frontiers in cardiovascular medicine · 2022
    Article
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

3 authors at 1 institution in 1 country.

Beatriz Delgado-ValeroDepartamento de Fisiología, Facultad de Medicina, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Universidad Complutense de Madrid, 28040 Madrid, Spain.ORCID 0000-0001-6147-5964
Victoria CachofeiroDepartamento de Fisiología, Facultad de Medicina, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Universidad Complutense de Madrid, 28040 Madrid, Spain.ORCID 0000-0001-6959-6293
Ernesto Martínez-MartínezDepartamento de Fisiología, Facultad de Medicina, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Universidad Complutense de Madrid, 28040 Madrid, Spain.ORCID 0000-0002-3011-2041
Universidad Complutense de Madrid · ES

Funding

Instituto de Salud Carlos III PI15/00742; PI18/00257; FI19/00277
6 · The paper itself

Abstract

Cardiorenal syndrome is a term that defines the complex bidirectional nature of the interaction between cardiac and renal disease. It is well established that patients with kidney disease have higher incidence of cardiovascular comorbidities and that renal dysfunction is a significant threat to the prognosis of patients with cardiac disease. Fibrosis is a common characteristic of organ injury progression that has been proposed not only as a marker but also as an important driver of the pathophysiology of cardiorenal syndromes. Due to the relevance of fibrosis, its study might give insight into the mechanisms and targets that could potentially be modulated to prevent fibrosis development. The aim of this review was to summarize some of the pathophysiological pathways involved in the fibrotic damage seen in cardiorenal syndromes, such as inflammation, oxidative stress and endoplasmic reticulum stress, which are known to be triggers and mediators of fibrosis.

Indexed as

AnimalsCardio-Renal SyndromeDisease ProgressionFibrosisHumansModels, Biologicalcardiorenal syndromeendoplasmic reticulum stressfibrosisheart failureinflammationkidney diseaseoxidative stress

Identifiers

PMID34359993
PMCPMC8307805
OpenAlexW3186464156

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.