Evidence map›Paper›PMID 16604332›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2006

Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy.

Gavin Y Oudit, Maria G Trivieri, Neelam Khaper, Peter P Liu, Peter H Backx

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01239901 (Iron-mediated Vascular Disease in Sickle Cell Disease.), which is not on this map. Cited by 91 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 3 pooled it
4.3field-weighted citation impact, top 5% 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.

NCT01239901 completednot on this mapstarted 2009, after this paper: background citation

Iron-mediated Vascular Disease in Sickle Cell Disease.

TypeobservationalSponsorChildren's Hospital Los AngelesRan2009 to 2018Enrolled150ConditionsSickle Cell Disease
3 · Its place in the literature

Who cites it

91 citing papers in PubMed, 3 syntheses or guidelines pooled it, 220 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Combined chelation therapy in thalassemia major for the treatment of severe myocardial siderosis with left ventricular dysfunction.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2008
    Trial
  10. Article
  11. Non-transferrin-bound iron uptake by cardiomyocytes.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Iron Metabolism in Cardiovascular Disease.Advances in experimental medicine and biology · 2025
    Review
  19. Cardiac Dysfunction in β-Thalassemia: A Narrative Review.Research in heart yield and translational medicine · 2025
    Review
  20. Review

31 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 3 institutions in 1 country.

Gavin Y OuditHeart and Stroke/Richard Lewar Centre of Excellence, University Health Network, University of Toronto, Ontario, M5S 3E2, Canada.
Maria G Trivieri
Neelam Khaper
Peter P Liu
Peter H Backx
University Health Network · CAHeart and Stroke Foundation · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive body iron or iron overload occurs under conditions such as primary (hereditary) hemochromatosis and secondary iron overload (hemosiderosis), which are reaching epidemic levels worldwide. Primary hemochromatosis is the most common genetic disorder with an allele frequency greater than 10% in individuals of European ancestry, while hemosiderosis is less common but associated with a much higher morbidity and mortality. Iron overload leads to iron deposition in many tissues especially the liver, brain, heart and endocrine tissues. Elevated cardiac iron leads to diastolic dysfunction, arrhythmias and dilated cardiomyopathy, and is the primary determinant of survival in patients with secondary iron overload as well as a leading cause of morbidity and mortality in primary hemochromatosis patients. In addition, iron-induced cardiac injury plays a role in acute iron toxicosis (iron poisoning), myocardial ischemia-reperfusion injury, Friedreich ataxia and neurodegenerative diseases. Patients with iron overload also routinely suffer from a range of endocrinopathies, including diabetes mellitus and anterior pituitary dysfunction. Despite clear connections between elevated iron and clinical disease, iron transport remains poorly understood. While low-capacity divalent metal and transferrin-bound transporters are critical under normal physiological conditions, L-type Ca2+ channels (LTCC) are high-capacity pathways of ferrous iron (Fe2+) uptake into cardiomyocytes especially under iron overload conditions. Fe2+ uptake through L-type Ca2+ channels may also be crucial in other excitable cells such as pancreatic beta cells, anterior pituitary cells and neurons. Consequently, LTCC blockers represent a potential new therapy to reduce the toxic effects of excess iron.

Indexed as

Biological TransportCalcium Channel BlockersCalcium Channels, L-TypeCardiomyopathiesCation Transport ProteinsEndocrine System DiseasesFerroportinHemochromatosisHumansIronMyocardiumPoisoningReceptors, TransferrinTransferrinCalcium Channel BlockersCalcium Channels, L-TypeCation Transport ProteinsFerroportinIronReceptors, TransferrinTransferrin

Identifiers

PMID16604332
PMCPMC7095819
OpenAlexW2165551729

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.