Evidence map›Paper›PMID 20615072›Full record

ReviewAntioxidants & redox signaling2011

Targeting Forkhead box O1 from the concept to metabolic diseases: lessons from mouse models.

Zhiyong Cheng, Morris F White

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing 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

105 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Molecular and Phenotypic Changes in FLExDUX4 Mice.Journal of personalized medicine · 2023
    Article
  10. The Pathogenesis of Diabetes.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Assessing the Activity of Transcription Factor FoxO1.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

45 more citing papers are in PubMed but not listed here.

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.

Zhiyong ChengDivision of Endocrinology, Howard Hughes Medical Institute, Harvard Medical School, Children's Hospital Boston, Boston, Massachusetts 02115, USA.
Morris F White

Funding

Regulating IRS-proteins by Ser/Thr PhosphorylationR01DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1992 to 2014
$5.0M
IRS-2 FUNCTION IN BETA CELL PHYSIOLOGYR01DK055326 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 2000 to 2010
$2.9M
INSULIN RECEPTOR REGULATION BY MULTISITE PHOSPHORYLATIONR29DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1987 to 1989
–
INTERACTION BETWEEN INSULIN RECEPTORS AND CELL PROTEINSR55DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1991 to 1991
–
NIDDK NIH HHS DK38712NIDDK NIH HHS DK55326NIDDK NIH HHS R01 DK038712
6 · The paper itself

Abstract

Forkhead box O (FOXO) transcription factors have been implicated in regulating the metabolism, cellular proliferation, stress resistance, apoptosis, and longevity. Through the insulin receptor substrate → phosphoinositide 3-kinase → Akt signal cascade, FOXO integrates insulin action with the systemic nutrient and energy homeostasis. Activation of FOXO1 in liver induces gluconeogenesis via phosphoenolpyruvate carboxykinase (PEPCK)/glucose 6-phosphate pathway, and disrupts mitochondrial metabolism and lipid metabolism via heme oxygenase 1/sirtuin 1/Ppargc1α pathway. In skeletal muscle, FOXO1 activation underpins the carbohydrate/lipid switch during fasting state. Inhibition of FOXO1 under physiological conditions accounts for maintenance of skeletal muscle mass/function and adipose differentiation. In pancreatic β-cells, nuclear translocation of FOXO1 antagonizes pancreatic and duodenal homeobox 1 and attenuates β-cells proliferation and insulin secretion. Regardless, FOXO1 promotes the proliferation of β-cells through induction of Cyclin D1 in low nutrition, and elicits antioxidant mechanism to protect against β-cell failure during oxidative insults. In the brain, FOXO1 controls food intake through transcriptional regulation of the orexigenic neuropeptide Y, agouti-related protein, and carboxypeptidase E. In this article, we review the role of FOXO1 in the regulation of metabolism and energy expenditure based on recent findings from mouse models, and discuss the therapeutic value of targeting FOXO1 in metabolic diseases.

Indexed as

Adipose TissueAnimalsBrainForkhead Transcription FactorsHumansMetabolic DiseasesMiceMuscle, SkeletalForkhead Transcription Factors

Identifiers

PMID20615072
PMCPMC3025764

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.