Evidence map›Paper›PMID 21163265›Full record

ReviewJournal of molecular and cellular cardiology2011

Targeting GSK-3 family members in the heart: a very sharp double-edged sword.

Hui Cheng, James Woodgett, Mia Maamari, Thomas Force

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. WNT Signaling in Cardiac and Vascular Disease.Pharmacological reviews · 2018
    Review
  16. Cyclin D2 is a critical mediator of exercise-induced cardiac hypertrophy.Experimental biology and medicine (Maywood, N.J.) · 2017
    Article
  17. Article
  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

4 authors at 2 institutions in 2 countries.

Hui ChengCenter for Translational Medicine and Cardiology Division, Thomas Jefferson University Hospital, Philadelphia, PA, USA. hui.cheng@jefferson.edu
James Woodgett
Mia Maamari
Thomas Force
Thomas Jefferson University Hospital · USLunenfeld-Tanenbaum Research Institute · CA

Funding

SIGNALING MECHANISMS GOVERNING CARDIAC HYPERTROPHYR01HL061688 · NHLBI · VANDERBILT UNIVERSITY · PI FORCE, THOMAS · 1999 to 2014
$5.7M
NHLBI NIH HHS R01 HL061688
6 · The paper itself

Abstract

The GSK-3 family of serine/threonine kinases, which is comprised of two isoforms (α and β), was initially identified as a negative regulator of glycogen synthase, the rate limiting enzyme of glycogen synthesis [1,2]. In the 30 years since its initial discovery, the family has been reported to regulate a host of additional cellular processes and, consequently, disease states such as bipolar disorders, diabetes, inflammatory diseases, cancer, and neurodegenerative diseases including Alzheimer's Disease and Parkinson's Disease [3,4]. As a result, there has been intense interest on the part of the pharmaceutical industry in developing small molecule antagonists of GSK-3. Herein, we will review the roles played by GSK-3s in the heart, focusing primarily on recent studies that have employed global and tissue-specific gene deletion. We will highlight roles in various pathologic processes, including pressure overload and ischemic injury, focusing on some striking isoform-specific effects of the family. Due to space limitations and/or the relatively limited data in gene-targeted mice, we will not be addressing the family's roles in ischemic pre-conditioning or its many interactions with various pro- and anti-apoptotic factors. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."

Indexed as

Molecular Targeted TherapyAnimalsCardiomegalyCell DifferentiationCell ProliferationDiabetes MellitusEmbryonic Stem CellsGene DeletionGlycogen Synthase Kinase 3HumansInsulin ResistanceMyocardial InfarctionMyocardiumMyocytes, CardiacProtein Kinase InhibitorsTranslational Research, BiomedicalGlycogen Synthase Kinase 3Protein Kinase Inhibitors

Identifiers

PMID21163265
PMCPMC3075376
OpenAlexW2091373459

What OpenQuestion holds

Textmetadata
LicenceTDM
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.