Evidence map›Paper›PMID 27613400›Full record

ReviewTrends in endocrinology and metabolism: TEM2016

Is REDD1 a Metabolic Éminence Grise?

Christopher Lipina, Harinder S Hundal

Open access · hybridAbstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
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  9. Article
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  11. Article
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  13. Article
  14. Observational
  15. Article
  16. Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. 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 1 institution in 1 country.

Christopher LipinaDivision of Cell Signalling and Immunology, Sir James Black Centre, School of Life Sciences, University of Dundee, Dundee, DD1 5EH, UK.
Harinder S HundalDivision of Cell Signalling and Immunology, Sir James Black Centre, School of Life Sciences, University of Dundee, Dundee, DD1 5EH, UK. Electronic address: h.s.hundal@dundee.ac.uk.
University of Dundee · GB

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

Regulated in development and DNA damage response 1 (REDD1) has been functionally linked to the control of diverse cellular processes due, at least in part, to its ability to repress mammalian or mechanistic Target of Rapamycin (mTOR) Complex-1 (mTORC1), a key protein complex controlled by hormonal and nutrient cues. Notably, emerging evidence suggests that REDD1 also regulates several pathways involved in modulating energy balance and metabolism. Herein, we discuss evidence implicating REDD1 as a key modulator of insulin action and metabolic function, including its potential contribution to mitochondrial biology and pancreatic islet function. Collectively, the available evidence suggests that REDD1 has a more prominent role in energy homeostasis than was previously thought, and implicates REDD1 as a potential therapeutic target for treatment of metabolic disorders.

Indexed as

AnimalsHumansMuscle, SkeletalObesityProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTranscription FactorsDDIT4 protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTranscription FactorsAktinsulinmTORobesityprotein kinase BREDD1skeletal muscle

Identifiers

PMID27613400
PMCPMC5119498
OpenAlexW2511340075

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.