ArticleCell transplantation
Knockdown of Tripartite Motif 8 Protects H9C2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of PI3K/Akt Signaling Pathway.
Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- TRIM52 Protects Against Doxorubicin-Induced Cardiac Inflammation, Oxidative Stress and Cardiac Injury.Journal of cellular and molecular medicine · 2026Article
- Article
- Identification of novel NRF2-dependent genes as regulators of lead and arsenic toxicity in neural progenitor cells.Journal of hazardous materials · 2024Article
- Review
- Article
- Salvianolic acid B inhibits myocardial I/R-induced ROS generation and cell apoptosis by regulating the TRIM8/GPX1 pathway.Pharmaceutical biology · 2022Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- Cross-Disorder Analysis of De Novo Variants Increases the Power of Prioritising Candidate Genes.Life (Basel, Switzerland) · 2021Article
- Emerging Roles of TRIM8 in Health and Disease.Cells · 2021Review
- Knockdown of TRIM8 Protects HK-2 Cells Against Hypoxia/Reoxygenation-Induced Injury by Inhibiting Oxidative Stress-Mediated Apoptosis and Pyroptosis via PI3K/Akt Signal Pathway.Drug design, development and therapy · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif 8 (TRIM8) is a member of the TRIM protein family that has been found to be implicated in cardiovascular disease. However, the role of TRIM8 in myocardial ischemia/reperfusion (I/R) has not been investigated. We aimed to explore the effect of TRIM8 on cardiomyocyte H9c2 cells exposed to hypoxia/reoxygenation (H/R). We found that TRIM8 expression was markedly upregulated in H9c2 cells after stimulation with H/R. Gain- and loss-of-function assays proved that TRIM8 knockdown improved cell viability of H/R-stimulated H9c2 cells. In addition, TRIM8 knockdown suppressed reactive oxygen species production and elevated the levels of superoxide dismutase and glutathione peroxidase. Knockdown of TRIM8 suppressed the caspase-3 activity, as well as caused significant increase in bcl-2 expression and decrease in bax expression. Furthermore, TRIM8 overexpression exhibited apposite effects with knockdown of TRIM8. Finally, knockdown of TRIM8 enhanced the activation of PI3K/Akt signaling pathway in H/R-stimulated H9c2 cells. Inhibition of PI3K/Akt by LY294002 reversed the effects of TRIM8 knockdown on cell viability, oxidative stress, and apoptosis of H9c2 cells. These present findings defined TRIM8 as a therapeutic target for attenuating and preventing myocardial I/R injury.
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