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August 7, 2010Journal of Molecular and Cellular CardiologyOpen Access

Myocardial stress remodelling after regional infarction is independent of glycogen synthase kinase-3 inactivation

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Why the study?

Is GSK-3 inactivation an obligatory signaling event in chronic post-infarct remodeling in mice?

Population

GSK-3α/β(Ala21/9) knockin (KI) mice encoding constitutively active GSK-3 isoforms and wild type mice

Comparison

Regional infarction vs Sham operation

Design

Preclinical

Follow-up

4 weeks

Authors

IWIan WebbPSPierre SicardJCJames Clark

Discussion

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Overview

GSK-3 inactivation is not obligatory for post-infarct remodeling in mice; leaves open its therapeutic relevance in human HF.

Structured PICO

Is GSK-3 inactivation an obligatory signaling event in chronic post-infarct remodeling in mice?

P
Population
GSK-3α/β(Ala21/9) knockin (KI) mice encoding constitutively active GSK-3 isoforms and wild type mice
I
Intervention
Regional infarction
C
Comparator
Sham operation
O
Outcome
Chronic remodeling response (normalized heart weight, left ventricular muscle volume, LV cavity dimensions, remote LV wall thickness, and contractile impairment)surrogate

GSK-3β phosphorylation and inactivation occurs with, but is not an obligatory signaling event in, chronic post-infarct remodeling in the mouse heart.

Cite This Study

Webb et al. (2010) studied this question.

synapsesocial.com/papers/6a707fa1ac440176ef2928b1https://doi.org/10.1016/j.yjmcc.2010.07.021
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Constitutive glycogen synthase kinase-3α/β activity protects against chronic β-adrenergic remodelling of the heart2010 · 31 citations
  2. 2Glycogen Synthase Kinase-3β Regulates Post–Myocardial Infarction Remodeling and Stress-Induced Cardiomyocyte Proliferation In Vivo2010 · 120 citations
  3. 3Distinct roles of GSK-3α and GSK-3β phosphorylation in the heart under pressure overload2008 · 137 citations
  4. 4Glycogen Synthase Kinase-3α Reduces Cardiac Growth and Pressure Overload-induced Cardiac Hypertrophy by Inhibition of Extracellular Signal-regulated Kinases2007 · 68 citations
  5. 5Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)2007 · 16 citations