ArticleCardiovascular toxicology2025
KLF9-Mediated Transcriptional Promotion of HMGB2 Accelerates Cardiomyocyte Apoptosis, Inflammation, and Ferroptosis in Myocardial Ischemia/Reperfusion Injury.
Article in Cardiovascular toxicology, 2025. 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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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Endothelial Klf9 fine-tunes Akt signaling to act as a transcriptional brake restraining retinal angiogenesis.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group protein B2 (HMGB2) has been confirmed to participate in regulating the process of myocardial ischemia/reperfusion (I/R) injury. However, the more roles and mechanisms of HMGB2 in myocardial I/R injury need to be further revealed. Cardiomyocytes (HL-1) were cultured under hypoxia/reoxygenation (H/R) conditions, and myocardial I/R injury mouse model was established by ligation of the left anterior descending coronary artery. The protein levels of HMGB2 and kruppel-like factor 9 (KLF9) were determined by western blot. Cell viability and apoptosis were examined by CCK8 assay and flow cytometry. The levels of inflammatory factors and ferroptosis-related markers were tested to assess cell inflammation and ferroptosis. The interaction between KLF9 and HMGB2 promoter was evaluated by ChIP assay and dual-luciferase reporter assay. HMGB2 was higher expressed in H/R-induced HL-1 cells and its silencing could suppress H/R-induced HL-1 cell apoptosis, inflammation, and ferroptosis. KLF9 had binding sites in HMGB2 promoter region, which could increase HMGB2 expression by enhancing its transcription. Silencing of KLF9 inhibited H/R-induced HL-1 cell apoptosis, inflammation, and ferroptosis, while these effects were reversed by overexpressing HMGB2. In addition, animal study revealed that interference of KLF9 alleviated myocardial tissues damage and fibrosis in I/R injury mice models by reducing HMGB2 expression. Collectively, our study indicated that KLF9 promoted myocardial I/R injury by aggravating cardiomyocyte apoptosis, inflammation, and ferroptosis through promoting HMGB2 transcription.
Indexed as
Identifiers
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Registered trials
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