Evidence map›Paper›PMID 28293076›Full record

ArticleBioinformation2016

Microarray Integrated Analysis of a Gene Network for the CD36 Myocardial Phenotype.

Imane Sabaouni, Brigitte Vannier, Ahmed Moussa, Azeddine Ibrahimi

Open access · hybridAbstract read
In one paragraph

Article in Bioinformation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

4 authors at 3 institutions in 2 countries.

Imane SabaouniMedical Biotechnology Lab (MedBiotech), Rabat Medical & Pharmacy School, Mohammed Vth University in Rabat, Morocco.
Brigitte VannierReceptors, Regulation and Tumor Cells (2RTC) Laboratory, University of Poitiers, France.
Ahmed MoussaLabTIC Laboratory, ENSA, Abdelmalek Essaadi University, Tangier, Morocco.
Azeddine IbrahimiMedical Biotechnology Lab (MedBiotech), Rabat Medical & Pharmacy School, Mohammed Vth University in Rabat, Morocco.
Mohammed V University · MAAbdelmalek Essaâdi University · MAUniversité de Poitiers · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD36 is a multifunctional membrane-type receptor glycoprotein that reacts with oxidized low-density lipoprotein and long-chain fatty acid (LCFA). However, much remains to be understood about the molecular mechanism of the cardio-myopathy observed in CD36-KO mice. In this study, we identify different genes pathways involved in response to CD36 cardio-myopathy phenotype by identifying the differences among biological processes, molecular pathways and networks of interactions that emerge from knocking CD3 and using different bioinformatics tools such as STRING, GeneMANIA and Cytoscape. We were able list all the CD36-regulated genes, their related function and their specific networks. Data analysis showed that CD36-regulated genes differentially expressed are involved in biological processes such as FA metabolism, angiogenesis/apoptosis and cell structure. These results provide the first look at mechanisms involved in CD36 deficiency and development of cardio-myopathy and the opportunity to identify new therapeutic targets.

Indexed as

angiogenesis/apoptosiscardio-myopathyCD36genes networksgenes pathwaysmetabolism

Identifiers

PMID28293076
PMCPMC5320929
OpenAlexW2584284147

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.