Evidence map›Paper›PMID 19498210›Full record

ReviewCirculation research2009

Role of glycogen synthase kinase-3beta in cardioprotection.

Magdalena Juhaszova, Dmitry B Zorov, Yael Yaniv, H Bradley Nuss, Su Wang, Steven J Sollott

Open access · greenAbstract readReview
In one paragraph

Review in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed
18.5field-weighted citation impact, top 1% 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

184 citing papers in PubMed, 348 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. PMCells · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Review

124 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

6 authors at 1 institution in 1 country.

Magdalena JuhaszovaLaboratory of Cardiovascular Science, Gerontology Research Center, Box 13, National Institute on Aging, NIH, Baltimore, Maryland 21224-6825, USA.
Dmitry B Zorov
Yael Yaniv
H Bradley Nuss
Su Wang
Steven J Sollott
National Institute on Aging · US

Funding

GSK3b mediates convergence of protection signaling to limit mitochondrial damage ZIAAG000823 · NIA · NATIONAL INSTITUTE ON AGING · PI SOLLOTT, STEVEN · 2009 to 2016
$6.8M
VASCULAR SMOOTH MUSCLE CELL DIFFERENTIATION ALTERS PDGF CALCIUM ION SIGNALLINGZ01AG000823 · NIA · NATIONAL INSTITUTE ON AGING · PI SOLLOTT, STEVEN J · 1994 to 2008
$1.4M
Intramural NIH HHS Z01 AG000823Intramural NIH HHS Z99 AG999999
6 · The paper itself

Abstract

Limitation of infarct size by ischemic/pharmacological pre- and postconditioning involves activation of a complex set of cell-signaling pathways. Multiple lines of evidence implicate the mitochondrial permeability transition pore (mPTP) as a key end effector of ischemic/pharmacological pre- and postconditioning. Increasing the ROS threshold for mPTP induction enhances the resistance of cardiomyocytes to oxidant stress and results in infarct size reduction. Here, we survey and synthesize the present knowledge about the role of glycogen synthase kinase (GSK)-3beta in cardioprotection, including pre- and postconditioning. Activation of a wide spectrum of cardioprotective signaling pathways is associated with phosphorylation and inhibition of a discrete pool of GSK-3beta relevant to mitochondrial signaling. Therefore, GSK-3beta has emerged as the integration point of many of these pathways and plays a central role in transferring protective signals downstream to target(s) that act at or in proximity to the mPTP. Bcl-2 family proteins and mPTP-regulatory elements, such as adenine nucleotide translocator and cyclophilin D (possibly voltage-dependent anion channel), may be the functional downstream target(s) of GSK-3beta. Gaining a better understanding of these interactions to control and prevent mPTP induction when appropriate will enable us to decrease the negative impact of the reperfusion-induced ROS burst on the fate of mitochondria and perhaps allow us to limit propagation of damage throughout and between cells and consequently, to better limit infarct size.

Indexed as

AnimalsCardiotonic AgentsCell DeathGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIschemic PreconditioningMammalsMitochondria, HeartMyocardial InfarctionMyocardial IschemiaMyocytes, CardiacProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesReceptors, Cell SurfaceReperfusion InjuryCardiotonic AgentsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesReceptors, Cell Surface

Identifiers

PMID19498210
PMCPMC2726042
OpenAlexW2160086057

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.