ArticleToxicology letters2019
Insights into the transcriptional regulation of the anthracycline reductase AKR7A2 in human cardiomyocytes.
Article in Toxicology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- METTL14 promotes doxorubicin-induced cardiomyocyte ferroptosis by regulating the KCNQ1OT1-miR-7-5p-TFRC axis.Cell biology and toxicology · 2023Article
- The Specific Binding and Promotion Effect of Azoles on Human Aldo-Keto Reductase 7A2.Metabolites · 2023Article
- Hsa-miR-223-3p participates in the process of anthracycline-induced cardiomyocyte damage by regulating NFIA gene.Open medicine (Warsaw, Poland) · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aldo-Keto Reductase Family 7 Member A2 (AKR7A2) is the most abundant anthracycline metabolizing enzyme in human myocardium. Myocardial AKR7A2 contributes to the synthesis of cardiotoxic C-13 anthracycline alcohol metabolites (e.g., doxorubicinol). The factors that govern the transcription of human AKR7A2 in cardiomyocytes remain largely unexplored. In this study, we performed the functional characterization of the AKR7A2 gene promoter in human AC16 cardiomyocytes. Experiments with gene reporter constructs and chromatin immunoprecipitation assays suggest that NF-κB binds to specific regions in the AKR7A2 promoter. Doxorubicin treatment modified the cellular levels of NF-κB and the expression of AKR7A2. Moreover, doxorubicin treatment led to changes in the pattern of AKR7A2 phosphorylation status. Our results suggest that AKR7A2 expression in human cardiomyocytes is mediated by NF-κB through conserved response elements in the proximal gene promoter region. This study provides the first insights into the functional characteristics of the human AKR7A2 gene promoter.
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