ArticleCell proliferation2021
Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction.
Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Research progress on the relationship between long QT syndrome (LQTS) and epilepsy: A review.Medicine · 2026Review
- STAT3/FoxO3a/Sirt1 pathway inhibition by ginsenoside Rc ameliorates cardiomyocyte damage in septic cardiomyopathy by altering macrophage polarization.Journal of molecular histology · 2025Article
- miR-29b-1-5p exacerbates myocardial injury induced by sepsis in a mouse model by targeting TERF2.Acta biochimica et biophysica Sinica · 2024Article
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- Identification of two novel ferroptosis-associated targets in sepsis-induced cardiac injury: Hmox1 and Slc7a11.Frontiers in cardiovascular medicine · 2023Article
- [FUT8 modulates galectin-3 expression to regulate TGF-β1-mediated fibrosis of lung fibroblasts].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Red Blood Cell Membrane-Camouflaged PLGA Nanoparticles Loaded With Basic Fibroblast Growth Factor for Attenuating Sepsis-Induced Cardiac Injury.Frontiers in pharmacology · 2022Article
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- Ferrostatin-1 alleviates lipopolysaccharide-induced cardiac dysfunction.Bioengineered · 2021Article
- microRNA-193-3p attenuates myocardial injury of mice with sepsis via STAT3/HMGB1 axis.Journal of translational medicine · 2021Article
- Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction.Cell proliferation · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesMyocardial dysfunction is a significant manifestation in sepsis, which results in high mortality. Even Kcnh2 has been hinted to associate with the pathological process, its involved signalling is still elusive. MATERIALS AND
methodsThe caecal ligation puncture (CLP) surgery or lipopolysaccharide (LPS) injection was performed to induce septic cardiac dysfunction. Western blotting was used to determine KCNH2 expression. Cardiac function was examined by echocardiography 6 hours after CLP and LPS injection in Kcnh2 knockout (Kcnh2
resultsSepsis could downregulate KCNH2 level in the rat heart, as well as in LPS-stimulated cardiomyocytes but not cardiac fibroblast. Defect of Kcnh2 (Kcnh2
conclusionKcnh2 plays a protection role in sepsis-induced cardiac dysfunction (SCID) via regulating FAK/AKT-FOXO3A to block LPS-induced myocardium apoptosis, indicating a potential effect of the potassium channels in pathophysiology of SCID.
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