ArticleJournal of cellular and molecular medicine2019
GSK-3β inhibition protects the rat heart from the lipopolysaccharide-induced inflammation injury via suppressing FOXO3A activity.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Targeting FOXO3 for the Management of Heart Failure: Current Evidence and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Research progress on the mechanism of FOXO protein in sepsis.Apoptosis : an international journal on programmed cell death · 2026Review
- STAT3/FoxO3a/Sirt1 pathway inhibition by ginsenoside Rc ameliorates cardiomyocyte damage in septic cardiomyopathy by altering macrophage polarization.Journal of molecular histology · 2025Article
- Pretreatment with interleukin-15 attenuates inflammation and apoptosis by inhibiting NF-κB signaling in sepsis-induced myocardial dysfunction.European journal of histochemistry : EJH · 2024Article
- miR-29b-1-5p exacerbates myocardial injury induced by sepsis in a mouse model by targeting TERF2.Acta biochimica et biophysica Sinica · 2024Article
- Fangji Fuling Decoction Alleviates Sepsis by Blocking MAPK14/FOXO3A Signaling Pathway.Chinese journal of integrative medicine · 2024Article
- Pterostilbene attenuates heart failure by inhibiting myocardial ferroptosis through SIRT1/GSK-3β/GPX4 signaling pathway.Heliyon · 2024Article
- Cardiac fibroblast GSK-3α aggravates ischemic cardiac injury by promoting fibrosis, inflammation, and impairing angiogenesis.Basic research in cardiology · 2023Article
- The β-catenin/CBP signaling axis participates in sepsis-induced inflammatory lung injury.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Mdivi-1 Modulates Macrophage/Microglial Polarization in Mice with EAE via the Inhibition of the TLR2/4-GSK3β-NF-κB Inflammatory Signaling Axis.Molecular neurobiology · 2022Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- Article
- Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction.Cell proliferation · 2021Article
- Beneficial role of oleuropein in sepsis-induced myocardial injury. Possible Involvement of GSK-3β/NF-kB pathway.Acta cirurgica brasileira · 2021Article
- Glycogen Synthase Kinase 3β Modulates the Inflammatory Response Activated by Bacteria, Viruses, and Parasites.Frontiers in immunology · 2021Review
- lncRNA NEAT1 mediates sepsis progression by regulating Irak2 via sponging miR-370-3p.Biology open · 2020Article
- GSK-3β inhibition protects the rat heart from the lipopolysaccharide-induced inflammation injury via suppressing FOXO3A activity.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced cardiac dysfunction represents a main cause of death in intensive care units. Previous studies have indicated that GSK-3β is involved in the modulation of sepsis. However, the signalling details of GSK-3β regulation in endotoxin lipopolysaccharide (LPS)-induced septic myocardial dysfunction are still unclear. Here, based on the rat septic myocardial injury model, we found that LPS could induce GSK-3β phosphorylation at its active site (Y216) and up-regulate FOXO3A level in primary cardiomyocytes. The FOXO3A expression was significantly reduced by GSK-3β inhibitors and further reversed through β-catenin knock-down. This pharmacological inhibition of GSK-3β attenuated the LPS-induced cell injury via mediating β-catenin signalling, which could be abolished by FOXO3A activation. In vivo, GSK-3β suppression consistently improved cardiac function and relieved heart injury induced by LPS. In addition, the increase in inflammatory cytokines in LPS-induced model was also blocked by inhibition of GSK-3β, which curbed both ERK and NF-κB pathways, and suppressed cardiomyocyte apoptosis via activating the AMP-activated protein kinase (AMPK). Our results demonstrate that GSK-3β inhibition attenuates myocardial injury induced by endotoxin that mediates the activation of FOXO3A, which suggests a potential target for the therapy of septic cardiac dysfunction.
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