ArticleCell death & disease2019
Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 1 of them a synthesis that pooled it.
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Who cites it
221 citing papers in PubMed, 1 synthesis or guideline pooled it, 349 citations in OpenAlex.
- Meta-Analysis of Extracellular Matrix Dynamics after Myocardial Infarction Using RNA-Sequencing Transcriptomic Database.International journal of molecular sciences · 2022Pooled it
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- SREBF2 promotes mitophagy and protects against ferroptosis via Cav-1-regulated PINK1/Parkin signaling in ischemic heart failure.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Targeting ferroptosis and oxidative stress crosstalk: a new frontier in stroke neuroprotection.Journal of molecular histology · 2026Review
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- Calycosin protects against post-myocardial infarction heart failure by activating the NRF2/HO-1 signaling pathway.Journal of thoracic disease · 2026Article
- Site-specific promoter hypermethylation of GPX4 in heart failure with reduced ejection fraction (HFrEF): nonlinear dose-response with hepatic and coagulation markers.Molecular biology reports · 2026Article
- Dapagliflozin confers protection against ferroptosis in cardiomyocyte via the inhibition of interferon-gamma pathway.Molecular biology reports · 2026Article
- Implications of ferritinophagy in cardiovascular diseases and its pharmacological modulation: underlying mechanisms and clinical translation strategies.Cellular & molecular biology letters · 2026Review
- A Comprehensive Bibliometric and Visual Analysis of EGR1 in Cardiovascular Disease.Molecular biotechnology · 2026Review
- Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging.Diagnostics (Basel, Switzerland) · 2026Review
- Growth Hormone-Releasing Peptide-6 (GHRP-6) Ameliorates Post-Infarct Ventricular Remodeling and Systolic Dysfunction in a Model of Permanent Coronary Ligation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation.Cell death discovery · 2026Review
- Ferroptosis in cardiovascular diseases: molecular mechanisms and a novel therapeutic target.Molecular biomedicine · 2026Review
- Mechanisms of the RGS12-GPX4-ACSL4 signaling axis in regulating ferroptosis during myocardial ischemia-reperfusion injury.Journal of anesthesia and translational medicine · 2026Review
- USP13 ameliorates myocardial infarction injury by inhibiting ferroptosis via stabilizing ALDOA.Redox biology · 2026Article
- Inhibition of Setd7 protects against cardiomyocyte hypertrophy via inhibiting lipid oxidation.Acta pharmacologica Sinica · 2026Article
- Potential ofFrontiers in immunology · 2026Article
- Matrine as a multi-disease regulator of ferroptosis: mechanisms, therapeutic applications, and toxicity management.Frontiers in pharmacology · 2026Review
161 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischaemic heart disease (IHD) is the leading cause of death worldwide. Although myocardial cell death plays a significant role in myocardial infarction (MI), its underlying mechanism remains to be elucidated. To understand the progression of MI and identify potential therapeutic targets, we performed tandem mass tag (TMT)-based quantitative proteomic analysis using an MI mouse model. Gene ontology (GO) analysis and gene set enrichment analysis (GSEA) revealed that the glutathione metabolic pathway and reactive oxygen species (ROS) pathway were significantly downregulated during MI. In particular, glutathione peroxidase 4 (GPX4), which protects cells from ferroptosis (an iron-dependent programme of regulated necrosis), was downregulated in the early and middle stages of MI. RNA-seq and qRT-PCR analyses suggested that GPX4 downregulation occurred at the transcriptional level. Depletion or inhibition of GPX4 using specific siRNA or the chemical inhibitor RSL3, respectively, resulted in the accumulation of lipid peroxide, leading to cell death by ferroptosis in H9c2 cardiomyoblasts. Although neonatal rat ventricular myocytes (NRVMs) were less sensitive to GPX4 inhibition than H9c2 cells, NRVMs rapidly underwent ferroptosis in response to GPX4 inhibition under cysteine deprivation. Our study suggests that downregulation of GPX4 during MI contributes to ferroptotic cell death in cardiomyocytes upon metabolic stress such as cysteine deprivation.
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