Evidence map›Paper›PMID 33387073›Full record

ReviewCurrent diabetes reports2021

The β-Cell Genomic Landscape in T1D: Implications for Disease Pathogenesis.

Mireia Ramos-Rodríguez, Beatriz Pérez-González, Lorenzo Pasquali

Abstract readReview
In one paragraph

Review in Current diabetes reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. GRP94 is indispensable for definitive endoderm specification of human induced pluripotent stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. β-Cell autophagy in the pathogenesis of type 1 diabetes.American journal of physiology. Endocrinology and metabolism · 2021
    Review
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.

Mireia Ramos-Rodríguez *Endocrine Regulatory Genomics, Department of Experimental & Health Sciences, University Pompeu Fabra, 08003, Barcelona, Spain.
Beatriz Pérez-González *Endocrine Regulatory Genomics, Department of Experimental & Health Sciences, University Pompeu Fabra, 08003, Barcelona, Spain.
Lorenzo PasqualiEndocrine Regulatory Genomics, Department of Experimental & Health Sciences, University Pompeu Fabra, 08003, Barcelona, Spain. lorenzo.pasquali@upf.edu.ORCID 0000-0003-2423-1826

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewType 1 diabetes (T1D) develops as a consequence of a combination of genetic predisposition and environmental factors. Combined, these events trigger an autoimmune disease that results in progressive loss of pancreatic β cells, leading to insulin deficiency. This article reviews the current knowledge on the genetics of T1D with a specific focus on genetic variation in pancreatic islet regulatory networks and its implication to T1D risk and disease development. RECENT

findingsAccumulating evidence suggest an active role of β cells in T1D pathogenesis. Based on such observation several studies aimed in mapping T1D risk variants acting at the β cell level. Such studies unravel T1D risk loci shared with type 2 diabetes (T2D) and T1D risk variants potentially interfering with β-cell responses to external stimuli. The characterization of regulatory genomics maps of disease-relevant states and cell types can be used to elucidate the mechanistic role of β cells in the pathogenesis of T1D.

Indexed as

Diabetes Mellitus, Type 1Diabetes Mellitus, Type 2Insulin-Secreting CellsIslets of LangerhansGenomicsHumansBeta cellsEpigenomicsHuman geneticsPancreatic isletsRegulatory genomicsType 1 diabetes

Identifiers

PMID33387073
PMCPMC7778620

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.