ArticleInternational journal of molecular medicine2016
HMGB1 induces apoptosis and EMT in association with increased autophagy following H/R injury in cardiomyocytes.
Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.NPJ cardiovascular health · 2026Article
- HMGB1: a multifaceted mediator of cell death pathways in cardiovascular diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- HMGB1/RAGE Signaling Regulates Th17/IL-17 and Its Role in Bronchial Epithelial-Mesenchymal Transformation.Current molecular medicine · 2024Article
- Use of Machine Learning for the Identification and Validation of Immunogenic Cell Death Biomarkers and Immunophenotypes in Coronary Artery Disease.Journal of inflammation research · 2024Article
- L-ascorbic acid could ameliorate the damage of myocardial microvascular endothelial cell caused by hypoxia-reoxygenation via targeting HMGB1.Journal of bioenergetics and biomembranes · 2023Article
- Autophagic degradation of CCN2 (cellular communication network factor 2) causes cardiotoxicity of sunitinib.Autophagy · 2022Article
- [Ginsenoside Rh2 inhibits renal fibrosis and renal cell apoptosis in rats with diabetic nephropathy by downregulating discoid domain receptor 1].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- miR-19a mitigates hypoxia/reoxygenation-induced injury by depressing CCL20 and inactivating MAPK pathway in human embryonic cardiomyocytes.Biotechnology letters · 2021Article
- CircPAN3 ameliorates myocardial ischaemia/reperfusion injury by targeting miR-421/Pink1 axis-mediated autophagy suppression.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- HMGB1 Mediated Inflammation and Autophagy Contribute to Endometriosis.Frontiers in endocrinology · 2021Article
- Dihydroartemisinin inhibits the migration of esophageal cancer cells by inducing autophagy.Oncology letters · 2020Article
- Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Berberine attenuates mitochondrial dysfunction by inducing autophagic flux in myocardial hypoxia/reoxygenation injury.Cell stress & chaperones · 2020Article
- The inhibition of miR‑101a‑3p alleviates H/R injury in H9C2 cells by regulating the JAK2/STAT3 pathway.Molecular medicine reports · 2020Article
- The Roles of Beclin 1 Expression in Gastric Cancer: A Marker for Carcinogenesis, Aggressive Behaviors and Favorable Prognosis, and a Target of Gene Therapy.Frontiers in oncology · 2020Article
- High-Mobility Group Box 1 Neutralization Prevents Chronic Cerebral Hypoperfusion-Induced Optic Tract Injuries in the White Matter Associated with Down-regulation of Inflammatory Responses.Cellular and molecular neurobiology · 2019Article
- HMGB1-RAGE Signaling Plays a Role in Organic Dust-Induced Microglial Activation and Neuroinflammation.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Transmembrane-4 L-six family member-1 (TM4SF1) promotes non-small cell lung cancer proliferation, invasion and chemo-resistance through regulating the DDR1/Akt/ERK-mTOR axis.Respiratory research · 2019Article
- Crosstalk between autophagy and epithelial-mesenchymal transition and its application in cancer therapy.Molecular cancer · 2019Review
- MicroRNAs as Potential Pharmaco-targets in Ischemia-Reperfusion Injury Compounded by Diabetes.Cells · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia/reoxygenation (H/R) is a critical factor in the pathogenesis of tissue injury following myocardial infarction (MI) which can lead to tissue damage and pathological remodeling. Therefore, it is necessary to try and prevent myocardial H/R injury in order to optimize the treatment of MI. This study aimed to explore the functions and molecular mechanisms of action of high mobility group box 1 (HMGB1) and its role in H/R injury to H9c2 cells. The mRNA expression of levels genes were detected by RT-qPCR. The protein levels were examined by western blot analysis. The Beclin 1 expression level was further determined by immunocytochemistry (ICC). In addition, an HMGB1 overexpression vector and a shRNA lentiviral vector were constructed in order to induce the overexpression and silencing of HMGB1, respectively. The apoptotic rate of the H9c2 cells was determined by flow cytometry. The expression of miR-210 was markedly increased following the exposure of the cells to H/R, thus indicating that the cell model of H/R injury was successfully established. In addition, an in vivo model of MI was also created using rats. The mRNA and protein level of HMGB1 was found to be upregulated in the myocardial tissue of the rats with MI and in the H9c2 cells subjected to H/R injury. HMGB1 promoted apoptosis by increasing the expression of cleaved caspase-3 and the apoptotic rate of the cells, while decreasing the expression of Bcl-2 during H/R in the H9c2 cells. HMGB1 promoted epithelial-to-mesenchymal transition (EMT) by reducing the protein level of the epithelial marker, E-cadherin, while increasing the expression of the mesenchymal markers, vimentin and fibroblast-specific protein (FSP), during H/R in the H9c2 cells. HMGB1 induced the apoptosis of the H9c2 cells and EMT following H/R in association with the induction of autophagy. HMGB1 induced autophagy by upregulating the expression of discoidin domain receptor 1 (DDR1) and downregulating the phosphorylation levels of mammalian target of rapamycin (mTOR). In conclusion, the findings of our study suggest that HMGB1 promotes apoptosis and EMT in association with the induction of autophagy through the upregulation of the expression of DDR1 and the downregulation of the phosphorylation of mTOR following H/R injury in H9c2 cells.
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