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December 31, 2014Circulation ResearchOpen Access

Deletion of GSK-3α specifically in cardiomyocytes attenuates ventricular remodeling and cardiac dysfunction after myocardial infarction, whereas specific deletion of GSK-3β in cardiac fibroblasts leads to fibrogenesis, left ventricular dysfunction, and excessive scarring.

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Population

Mouse models with cardiomyocyte- and fibroblast-specific conditional gene deletion of GSK-3

Design

Review

Authors

HLHind LalFAFirdos AhmadJWJames R. Woodgett

Discussion

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Overview

Cell-specific GSK-3 effects caution against nonselective inhibition post-MI; leaves open isoform-targeted strategies for prospective validation.

Structured PICO

P
Population
Mouse models with cardiomyocyte- and fibroblast-specific conditional gene deletion of GSK-3
I
Intervention
Deletion or inhibition of GSK-3 isoforms (GSK-3α and GSK-3β)
O
Outcome
Ventricular remodeling, cardiac dysfunction, myocardial fibrosis, and cardiomyocyte proliferation

GSK-3 isoforms have distinct and cell-specific roles in the heart, highlighting the complexity of targeting this pathway for myocardial diseases.

Cite This Study

Lal et al. (2014) studied this question.

synapsesocial.com/papers/6a707fa1ac440176ef2928aehttps://doi.org/10.1161/circresaha.116.303613
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Also Consider

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

  1. 1Cardiac Fibroblast Glycogen Synthase Kinase-3β Regulates Ventricular Remodeling and Dysfunction in Ischemic Heart2014 · 172 citations
  2. 2Cardiac fibroblast GSK-3α mediates adverse myocardial fibrosis via IL-11 and ERK pathway2021 · 1 citations
  3. 3GSK-3α directly regulates β-adrenergic signaling and the response of the heart to hemodynamic stress in mice2010 · 67 citations
  4. 4Fibroblast GSK-3α Promotes Fibrosis via RAF-MEK-ERK Pathway in the Injured Heart2022 · 81 citations
  5. 5Inhibition of GSK-3 to induce cardiomyocyte proliferation: a recipe for <i>in situ</i> cardiac regeneration2018 · 45 citations