Evidence map›Paper›PMID 31313216›Full record

ReviewGeroScience2019

An expanding GSK3 network: implications for aging research.

Dylan C Souder, Rozalyn M Anderson

Open access · bronzeAbstract readReview
In one paragraph

Review in GeroScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Intracellular pH dynamics promotes zebrafish larval tail regeneration.bioRxiv : the preprint server for biology · 2026
    Article
  4. GSK-3β coordinates axonal microtubule organization through Shot and Tau.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Applications of artificial intelligence in drug discovery for neurological diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. The Change Rate of theBiology · 2024
    Article
  13. Review
  14. Deletion ofInternational journal of molecular sciences · 2024
    Article
  15. Article
  16. Review
  17. Nuclear face of Tau: an inside player in neurodegeneration.Acta neuropathologica communications · 2023
    Review
  18. Article
  19. Article
  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.

Dylan C SouderDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin, Madison, WI, 53705, USA.
Rozalyn M AndersonDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin, Madison, WI, 53705, USA. rozalyn.anderson@wisc.edu.ORCID 0000-0002-0864-7998
University of Wisconsin–Madison · US

Funding

Biology of Aging and Age-Related Diseases Training GrantT32AG000213 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Rozalyn M. Anderson, Sanjay Asthana · 1991 to 2026
$9.9M
Dietary Restriction and Aging in Rhesus MonkeysR01AG040178 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI ANDERSON, ROZALYN M., COLMAN, RICKI J · 2011 to 2020
$5.8M
Acetyl-CoA flux and mitochondrial adaptation: a pathogenic role in aging and AD?RF1AG057408 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI ANDERSON, ROZALYN M., PUGLIELLI, LUIGI · 2017 to 2017
$3.5M
NIA NIH HHS AG000213NIA NIH HHS AG057408NIA NIH HHS RF1 AG057408NIA NIH HHS T32 AG000213
6 · The paper itself

Abstract

The last few decades of longevity research have been very exciting. We now know that longevity and healthspan can be manipulated across species, from unicellular eukaryotes to nonhuman primates, and that while aging itself is inevitable, how we age is malleable. Numerous dietary, genetic, and pharmacological studies now point to links between metabolism and growth regulation as a central aspect in determining longevity and, perhaps more importantly, health with advancing age. Here, we focus on a relatively new player in aging studies GSK3, glycogen synthase kinase, a key factor in growth and metabolism whose name fails to convey the extensive breadth of its role in cellular adaptation. First, we provide a brief overview of GSK3, touching on those aspects that are likely relevant to aging. Then, we outline the role of GSK3 in cellular functions including growth signaling, cell fate, and metabolism. Next, we describe evidence demonstrating a direct role for GSK3 in a range of age-related diseases, despite the fact that they differ considerably in their etiology and pathology. Finally, we discuss the role that GSK3 may play in normative aging and how GSK3 might be a suitable target to oppose age-related disease vulnerability.

Indexed as

AgingAlzheimer DiseaseAnimalsCell ProliferationCell SurvivalCellular SenescenceEnergy MetabolismGlycogen Synthase Kinase 3HumansInflammationNeoplasmsPhosphorylationSignal TransductionTOR Serine-Threonine KinasesGlycogen Synthase Kinase 3MTOR protein, humanTOR Serine-Threonine KinasesAge-related diseaseAgingGlycogen synthase kinase 3GSK3Metabolism

Identifiers

PMID31313216
PMCPMC6815315
OpenAlexW2961177566

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.