ArticleJournal of the American Heart Association2021
Excessive Hypoxia-Inducible Factor-1α Expression Induces Cardiac Rupture via p53-Dependent Apoptosis After Myocardial Infarction.
Article in Journal of the American Heart Association, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- [Effects of exosomes derived from normoxic or hypoxic human umbilical vein endothelial cells on hypoxia-induced cardiomyocyte injury and cardiac fibroblast activationNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- LncRNAiScience · 2026Article
- Role of P2X7 Receptor on Hypoxia-Induced Vascular Endothelial Growth Factor Gene Expression in H9c2 Rat Cardiomyocytes.Journal of cardiovascular development and disease · 2025Article
- Inflammation-resolution signalling in cardiac repair, remodelling, and heart failure.European heart journal open · 2025Review
- Excessive HIF-1α driven by phospholipid metabolism causes septic cardiomyopathy through cytopathic hypoxia.Nature cardiovascular research · 2025Article
- Biological function of RNA-binding proteins in myocardial infarction: a potential emerging therapeutic limelight.Cell & bioscience · 2025Review
- A cardiac fibroblast-enriched micropeptide regulates inflammation in ischemia/reperfusion injury.JCI insight · 2025Article
- Contribution of hypoxia-inducible factor 1alpha to pathogenesis of sarcomeric hypertrophic cardiomyopathy.Scientific reports · 2025Article
- Synergistic effect of Hypoxic Conditioning and Cell-Tethering Colloidal Gels enhanced Productivity of MSC Paracrine Factors and Accelerated Vessel Regeneration.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- FTO suppresses cardiac fibrosis after myocardial infarction via mMolecular medicine (Cambridge, Mass.) · 2024Article
- Injectable Self-Oxygenating Cardio-Protective and Tissue Adhesive Silk-Based Hydrogel for Alleviating Ischemia After Mi Injury.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
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- Article
- Raspberry polyphenols target molecular pathways of heart failure.The Journal of nutritional biochemistry · 2024Article
- Deferasirox Targeting Ferroptosis Synergistically Ameliorates Myocardial Ischemia Reperfusion Injury in Conjunction With Cyclosporine A.Journal of the American Heart Association · 2024Article
- Inhibition of Pyruvate kinase M2 (PKM2) by shikonin attenuates isoproterenol-induced acute myocardial infarction via reduction in inflammation, hypoxia, apoptosis, and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- M1 macrophage-derived exosomes promote autoimmune liver injury by transferring long noncoding RNA H19 to hepatocytes.MedComm · 2023Article
- Guanxin V attenuates myocardial ischaemia reperfusion injury through regulating iron homeostasis.Pharmaceutical biology · 2022Article
- Immunomodulatory Cell Therapy Using αGalCer-Pulsed Dendritic Cells Ameliorates Heart Failure in a Murine Dilated Cardiomyopathy Model.Circulation. Heart failure · 2022Article
- Iron Overload via Heme Degradation in the Endoplasmic Reticulum Triggers Ferroptosis in Myocardial Ischemia-Reperfusion Injury.JACC. Basic to translational science · 2022Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Apoptosis plays a pivotal role in cardiac rupture after myocardial infarction (MI), and p53 is a key molecule in apoptosis during cardiac rupture. Hif-1α (hypoxia-inducible factor-1α), upregulated under hypoxia, is a known p53 inducer. However, the role of Hif-1α in the regulatory mechanisms underlying p53 upregulation, apoptosis, and cardiac rupture after MI is unclear. Methods and Results We induced MI in mice by ligating the left anterior descending artery. Hif-1α and p53 expressions were upregulated in the border zone at day 5 after MI, accompanied by apoptosis. In rat neonatal cardiomyocytes, treatment with cobalt chloride (500 μmol/L), which mimics severe hypoxia by inhibiting PHD (prolyl hydroxylase domain-containing protein), increased Hif-1α and p53, accompanied by myocyte death with caspase-3 cleavage. Silencing Hif-1α or p53 inhibited caspase-3 cleavage, and completely prevented myocyte death under PHD inhibition. In cardiac-specific Hif-1α hetero-knockout mice, expression of p53 and cleavage of caspase-3 and poly (ADP-ribose) polymerase were reduced, and apoptosis was suppressed on day 5. Furthermore, the cleavage of caspase-8 and IL-1β (interleukin-1β) was also suppressed in hetero knockout mice, accompanied by reduced macrophage infiltration and matrix metalloproteinase/tissue inhibitor of metalloproteinase activation. Although there was no intergroup difference in infarct size, the cardiac rupture and survival rates were significantly improved in the hetero knockout mice until day 10 after MI. Conclusions Hif-1α plays a pivotal role in apoptosis, inflammation, and cardiac rupture after MI, in which p53 is a critical mediator, and may be a prospective therapeutic target for preventing cardiac rupture.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.