ArticleJournal of geriatric cardiology : JGC2024
Aldo-Keto reductase 1C3 reduces myocardial cell damage after acute myocardial infarction by activating the Kelch-like ECH-associated protein 1-nuclear factor erythroid 2-related factor 2-antioxidant response element pathway to inhibit ferroptosis.
Article in Journal of geriatric cardiology : JGC, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Eleutheroside E Ameliorates D-Gal-Induced Senescence in Human Skin Fibroblasts Through PI3K/AKT Signaling.Current issues in molecular biology · 2025Article
- Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
Background: Acute myocardial infarction (AMI) is a high-risk cardiovascular condition associated with increased cellular damage and oxidative stress. Aldo-Keto Reductase 1C3 (AKR1C3) is a stress-regulating gene. Nevertheless, its specific role and mechanisms regarding AMI remain unclear. Methods: We assessed cardiac function through echocardiography; tissue damage was evaluated using Hematoxylin and Eosin (HE) and Masson trichrome staining. AKR1C3 expression levels were measured through Reverse transcription-quantitative polymerase chain reaction and western blot. Assessed cell viability using Cell Counting Kit-8 and lactate dehydrogenase (LDH) assays. The extent of ferroptosis was determined by measuring the levels of Fe Results: The rats in the AMI group displayed reduced heart function, more tissue damage, and lower AKR1C3 expression compared to the Sham group. Similarly, hypoxia-treated H9C2 cells showed reduced viability, and decreased AKR1C3 expression. Overexpressing AKR1C3 in H9C2 cells enhanced viability. Knocking down AKR1C3 exhibited the opposite effect. Of the inhibitors tested, Ferrostatin-1 most effectively restored cell viability in hypoxia-treated H9C2 cells. Moreover, H9C2 cells subjected to hypoxia suggested Keap1-Nrf2-ARE pathway inhibition. Overexpressing AKR1C3 reduced ferroptosis and activated the Keap1-Nrf2-ARE pathway in hypoxia-treated cells, knocking down AKR1C3 exhibited the opposite effect. Further experiments using ML385 in hypoxia-treated H9C2 cells with overexpressed AKR1C3 showed decreased viability and increased ferroptosis compared to the control. Using (R)-Sulforaphane in hypoxia-treated H9C2 cells with knocked-down AKR1C3 exhibited the opposite effect. Conclusion: This study's findings indicate that AKR1C3 plays a role in regulating ferroptosis in myocardial cells, with the Keap1-Nrf2-ARE pathway likely being a key mechanism behind it.
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Registered trials
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