Evidence map›Paper›PMID 24127137›Full record

ArticleCurrent diabetes reports2013

Bridging the gap between genetic associations and molecular mechanisms for type 2 diabetes.

Hui Jin Ng, Anna L Gloyn

Abstract read
PubMed Publisher
In one paragraph

Article in Current diabetes reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. IMPC impact on preclinical mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  2. Review
  3. Article
  4. The pancreatic β cell: recent insights from human genetics.Trends in endocrinology and metabolism: TEM · 2014
    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

2 authors at 2 institutions in 1 country.

Hui Jin NgOxford Centre for Diabetes, Endocrinology & Metabolism, Churchill Hospital, University of Oxford, Oxford, OX3 7LE, UK, natasha.ng@ocdem.ox.ac.uk.
Anna L Gloyn
Churchill Hospital · GBOxford Centre for Diabetes, Endocrinology and Metabolism · GB

Funding

Wellcome Trust 095101
6 · The paper itself

Abstract

Type 2 diabetes is a global pandemic for which there is currently no disease-modifying treatment. New and targeted therapeutics are greatly needed, but progress in identifying novel targets for therapeutic intervention is severely hampered by poor understanding of disease pathogenesis. Over the past 6 years, the success of genome-wide association studies has led to an unprecedented increase in the number of loci robustly associating with type 2 diabetes risk. Each of these signals offers the opportunity to uncover biological insights into disease pathogenesis, which, if harnessed effectively, hold the promise to deliver new pathways for therapeutic intervention, strategies for patient stratification, and potentially, biomarkers for identifying those at greatest risk of developing diabetes. We review the progress that has been made and the approaches being adopted and discuss the inherent challenges in moving from association signals, which largely map to poorly annotated sequence, to transcripts, mechanisms, and disease biology.

Indexed as

AnimalsDiabetes Mellitus, Type 2DNA MethylationGenome-Wide Association StudyHumansMicroRNAsMicroRNAs

Identifiers

PMID24127137
OpenAlexW1999087259

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.