Evidence map›Paper›PMID 19181781›Full record

ReviewHaematologica2009

Molecular basis of inherited microcytic anemia due to defects in iron acquisition or heme synthesis.

Achille Iolascon, Luigia De Falco, Carole Beaumont

Open access · goldAbstract readReview
In one paragraph

Review in Haematologica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 148 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Molecular Characterization of Three Novel Large Deletions Causing αInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Compound Heterozygosity forFrontiers in genetics · 2021
    Article
  16. Inherited microcytic anemias.Hematology. American Society of Hematology. Education Program · 2020
    Review
  17. Inherited iron overload disorders.Translational gastroenterology and hepatology · 2020
    Review
  18. Article
  19. Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019
    Review
  20. 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 2 institutions in 2 countries.

Achille IolasconDepartment of Biochemistry and Medical Biotechnologies, University Federico II, Naples, Italy. iolascon@dbbm.unina.it
Luigia De Falco
Carole Beaumont
Federico II University Hospital · ITInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microcytic anemia is the most commonly encountered anemia in general medical practice. Nutritional iron deficiency and beta thalassemia trait are the primary causes in pediatrics, whereas bleeding disorders and anemia of chronic disease are common in adulthood. Microcytic hypochromic anemia can result from a defect in globin genes, in heme synthesis, in iron availability or in iron acquisition by the erythroid precursors. These microcytic anemia can be sideroblastic or not, a trait which reflects the implications of different gene abnormalities. Iron is a trace element that may act as a redox component and therefore is integral to vital biological processes that require the transfer of electrons as in oxygen transport, oxidative phosphorylation, DNA biosynthesis and xenobiotic metabolism. However, it can also be pro-oxidant and to avoid its toxicity, iron metabolism is strictly controlled and failure of these control systems could induce iron overload or iron deficient anemia. During the past few years, several new discoveries mostly arising from human patients or mouse models have highlighted the implication of iron metabolism components in hereditary microcytic anemia, from intestinal absorption to its final inclusion into heme. In this paper we will review the new information available on the iron acquisition pathway by developing erythrocytes and its regulation, and we will consider only inherited microcytosis due to heme synthesis or to iron metabolism defects. This information could be useful in the diagnosis and classification of these microcytic anemias.

Indexed as

5-Aminolevulinate SynthetaseAnemiaAnemia, HypochromicAnemia, SideroblasticAnimalsHemeHumansIronModels, BiologicalMutation5-Aminolevulinate SynthetaseALAS2 protein, humanHemeIron

Identifiers

PMID19181781
PMCPMC2649346
OpenAlexW2113475611

What OpenQuestion holds

Textmetadata
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.