Evidence map›Paper›PMID 31116982›Full record

ArticleCell reports2019

β Cell Hypoxia-Inducible Factor-1α Is Required for the Prevention of Type 1 Diabetes.

Amit Lalwani, Joanna Warren, David Liuwantara, Wayne J Hawthorne, Philip J O'Connell, Frank J Gonzalez, Rebecca A Stokes, Jennifer Chen, D Ross Laybutt, Maria E Craig and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Roles of β-Cell Hypoxia in the Progression of Type 2 Diabetes.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Hypoxia-inducible factors and diabetes.The Journal of clinical investigation · 2020
    Review
  14. Article
  15. Article
  16. 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

13 authors at 4 institutions in 2 countries.

Amit LalwaniCenter for Diabetes, Obesity, and Endocrinology (CDOE), The Westmead Institute for Medical Research (WIMR), The University of Sydney, Sydney, NSW, Australia; Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia.
Joanna WarrenMucosal Autoimmunity, Garvan Institute of Medical Research, Sydney, NSW, Australia.
David LiuwantaraNational Pancreas Transplant Unit (NPTU), Westmead Hospital, Sydney, NSW, Australia.
Wayne J HawthorneFaculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia; National Pancreas Transplant Unit (NPTU), Westmead Hospital, Sydney, NSW, Australia.
Philip J O'ConnellNational Pancreas Transplant Unit (NPTU), Westmead Hospital, Sydney, NSW, Australia.
Frank J GonzalezLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Rebecca A StokesCenter for Diabetes, Obesity, and Endocrinology (CDOE), The Westmead Institute for Medical Research (WIMR), The University of Sydney, Sydney, NSW, Australia.
Jennifer ChenCenter for Diabetes, Obesity, and Endocrinology (CDOE), The Westmead Institute for Medical Research (WIMR), The University of Sydney, Sydney, NSW, Australia.
D Ross LaybuttIslet Biology, Garvan Institute of Medical Research, Sydney, NSW, Australia.
Maria E CraigFaculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia; The Children's Hospital at Westmead, Sydney, NSW, Australia; School of Women's and Children's Health, University of New South Wales, Kensington, NSW, Australia.
Michael M SwarbrickCenter for Diabetes, Obesity, and Endocrinology (CDOE), The Westmead Institute for Medical Research (WIMR), The University of Sydney, Sydney, NSW, Australia; School of Medical Sciences, University of New South Wales, Kensington, NSW, Australia.
Cecile KingMucosal Autoimmunity, Garvan Institute of Medical Research, Sydney, NSW, Australia.
Jenny E GuntonCenter for Diabetes, Obesity, and Endocrinology (CDOE), The Westmead Institute for Medical Research (WIMR), The University of Sydney, Sydney, NSW, Australia; Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia; St Vincent's Clinical School, University of New South Wales, Kensington, NSW, Australia; Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, NSW, Australia. Electronic address: jenny.gunton@sydney.edu.au.
The University of Sydney · AUGarvan Institute of Medical Research · AUWestmead Hospital · AUNational Cancer Institute · US

Funding

Xenobiotic receptorsZIABC005562 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$26.9M
Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
Intramural NIH HHS ZIA BC005562Intramural NIH HHS ZIA BC005708
6 · The paper itself

Abstract

The development of autoimmune disease type 1 diabetes (T1D) is determined by both genetic background and environmental factors. Environmental triggers include RNA viruses, particularly coxsackievirus (CV), but how they induce T1D is not understood. Here, we demonstrate that deletion of the transcription factor hypoxia-inducible factor-1α (HIF-1α) from β cells increases the susceptibility of non-obese diabetic (NOD) mice to environmentally triggered T1D from coxsackieviruses and the β cell toxin streptozotocin. Similarly, knockdown of HIF-1α in human islets leads to a poorer response to coxsackievirus infection. Studies in coxsackievirus-infected islets demonstrate that lack of HIF-1α leads to impaired viral clearance, increased viral load, inflammation, pancreatitis, and loss of β cell mass. These findings show an important role for β cells and, specifically, lack of β cell HIF-1α in the development of T1D. These data suggest new strategies for the prevention of T1D.

Indexed as

AnimalsApoptosisDiabetes Mellitus, Type 1HumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiceHypoxia-Inducible Factor 1, alpha Subunitapoptosisautoimmunitybeta-cellcoxsackievirusinflammationstreptozotocintype 1 diabetes

Identifiers

PMID31116982
PMCPMC6661122
OpenAlexW2946348635

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.