Evidence map›Paper›PMID 25878762›Full record

ReviewOxidative medicine and cellular longevity2015

Iron-induced damage in cardiomyopathy: oxidative-dependent and independent mechanisms.

Elena Gammella, Stefania Recalcati, Ilona Rybinska, Paolo Buratti, Gaetano Cairo

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Review of ferroptosis in colorectal cancer: Friends or foes?World journal of gastroenterology · 2023
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Metallic nanomedicine in cancer immunotherapy.Acta pharmaceutica Sinica. B · 2025
    Review
  9. Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

16 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

5 authors at 1 institution in 1 country.

Elena GammellaDepartment of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy.
Stefania RecalcatiDepartment of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy.
Ilona RybinskaDepartment of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy.
Paolo BurattiDepartment of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy.
Gaetano CairoDepartment of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy.
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The high incidence of cardiomyopathy in patients with hemosiderosis, particularly in transfusional iron overload, strongly indicates that iron accumulation in the heart plays a major role in the process leading to heart failure. In this context, iron-mediated generation of noxious reactive oxygen species is believed to be the most important pathogenetic mechanism determining cardiomyocyte damage, the initiating event of a pathologic progression involving apoptosis, fibrosis, and ultimately cardiac dysfunction. However, recent findings suggest that additional mechanisms involving subcellular organelles and inflammatory mediators are important factors in the development of this disease. Moreover, excess iron can amplify the cardiotoxic effect of other agents or events. Finally, subcellular misdistribution of iron within cardiomyocytes may represent an additional pathway leading to cardiac injury. Recent advances in imaging techniques and chelators development remarkably improved cardiac iron overload detection and treatment, respectively. However, increased understanding of the pathogenic mechanisms of iron overload cardiomyopathy is needed to pave the way for the development of improved therapeutic strategies.

Indexed as

AnimalsCardiomyopathiesDeferoxamineDisease Models, AnimalHumansIronIron OverloadIron-Regulatory ProteinsOxidative StressReactive Oxygen SpeciesSiderophoresDeferoxamineIronIron-Regulatory ProteinsReactive Oxygen SpeciesSiderophores

Identifiers

PMID25878762
PMCPMC4387903
OpenAlexW1973152120

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.