Evidence map›Paper›PMID 27579499›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Why is an energy metabolic defect the common outcome in BMFS?

Paolo Degan, Silvia Ravera, Enrico Cappelli

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Fanconi anemia: from DNA repair to metabolism.European journal of human genetics : EJHG · 2018
    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 3 institutions in 1 country.

Paolo Degana S. C. Mutagenesis, IRCCS AOU San Martino - IST (Istituto Nazionale per la Ricerca sul Cancro), CBA Torre A2 , Genova , Italy.
Silvia Raverab DIFAR-Biochemistry Lab., Department of Pharmacy, University of Genova , Genova , Italy.
Enrico Cappellic Hematology Unit, Istituto Giannina Gaslini , Genova , Italy.
Istituto Giannina Gaslini · ITOspedale Policlinico San Martino · ITUniversity of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inherited bone marrow failure syndromes (BMFS) are rare, distressing, inherited blood disorders of children. Although the genetic origin of these pathologies involves genes with different functions, all are associated with progressive haematopoietic impairment and an excessive risk of malignancies. Defects in energy metabolism induce oxidative stress, impaired energy production and an unbalanced ratio between ATP and AMP. This assumes an important role in self-renewal and differentiation in haematopoietic stem cells (HSC) and can play an important role in bone marrow failure. Defects in energetic/respiratory metabolism, in particular in FA and SDS cells, have been described recently and seem to be a pertinent argument in the discussion of the haematopoietic defect in BMFS, as an alternative to the hypotheses already established on this subject, which may shed new light on the evolution of these diseases.

Indexed as

Energy MetabolismAnemia, AplasticBone Marrow DiseasesBone Marrow Failure DisordersDNA DamageHematopoietic Stem CellsHemoglobinuria, ParoxysmalHumansModels, BiologicalStem Cell NicheBone marrow failurescancer prone diseasesenergy metabolismhematopoietic stem cellsoxidative stress

Identifiers

PMID27579499
PMCPMC5053575
OpenAlexW2513548408

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.