ArticleThe Journal of international medical research2020
Notch signaling is involved in the antiapoptotic effects of liraglutide on rat H9c2 cardiomyocytes exposed to hypoxia followed by reoxygenation.
Article in The Journal of international medical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Liraglutide Protects Cardiomyocytes against Isoprenaline-Induced Apoptosis in Experimental Takotsubo Syndrome.Biomedicines · 2024Article
- Cyclic Adenosine Monophosphate in Cardiac and Sympathoadrenal GLP-1 Receptor Signaling: Focus on Anti-Inflammatory Effects.Pharmaceutics · 2024Review
- Peptides Are Cardioprotective Drugs of the Future: The Receptor and Signaling Mechanisms of the Cardioprotective Effect of Glucagon-like Peptide-1 Receptor Agonists.International journal of molecular sciences · 2024Review
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- GLP-1 receptor agonists (GLP-1RAs): cardiovascular actions and therapeutic potential.International journal of biological sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLiraglutide (Lir) protects cardiomyocytes against high glucose-induced myocardial damage. This study investigated whether Notch signaling participated in the antiapoptotic effects of Lir on rat H9c2 cardiomyocytes subjected to hypoxia followed by reoxygenation (H/R).
methodsWe used H9c2 rat cardiomyocytes as a model of H/R and measured viability, apoptosis, and expression of the apoptotic genes Bax and Bcl-2 and Notch signaling genes Notch1 and Jagged1. Notch1 was depleted by siRNA to test the effect of Notch1 deficiency on the antiapoptotic effects of Lir on H/R-treated H9c2 cardiomyocytes.
resultsAfter H/R treatment, viability was significantly decreased, and the apoptosis rate was greater in the H/R group than in the control (CT). Lir at 50, 100, and 200 nM significantly increased viability and decreased apoptosis in H/R-treated H9c2 cells. Treatment with 50 nM Lir for 2 hours before H/R significantly increased the expression levels of Notch1, Jagged1, and Bcl-2 compared with the CT levels. Bax was downregulated, which indicated that Lir activated Notch signaling and inhibited apoptosis. Notch1 depletion partially abolished the antiapoptotic effect of Lir on H/R-treated H9c2 cells by altering apoptotic gene expression.
conclusionLir activated Notch signaling, which was responsible for the antiapoptotic effect of Lir on H9c2 cardiomyocytes.
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