ArticleFrontiers in pharmacology2022
Propofol Protects Myocardium From Ischemia/Reperfusion Injury by Inhibiting Ferroptosis Through the AKT/p53 Signaling Pathway.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 65 citations in OpenAlex.
- Clinical implications of ferroptosis in critical illness: a narrative review.Journal of intensive care · 2026Review
- Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging.Diagnostics (Basel, Switzerland) · 2026Review
- Ferroptosis in cardiovascular diseases: molecular mechanisms and a novel therapeutic target.Molecular biomedicine · 2026Review
- Lacylation of Stearoyl-CoA Desaturase-1 Contributes to the Myocardial Ischemia-Reperfusion Injury Through Regulating Wnt/β-Catenin Signaling.Journal of cardiovascular translational research · 2026Article
- Ciprofol attenuates cerebral Ischemia‒reperfusion injury in rats by inhibiting ferroptosis through upregulating AMPK.Scientific reports · 2026Article
- Concurrent activation of multiple programmed cell death pathways predicts 28-day mortality in pediatric sepsis: a retrospective PICU cohort study with differential sedative agent use between survivors and non-survivors.Frontiers in cell and developmental biology · 2026Article
- IGFBP2 plays a key role in aerobic exercise-mediated inhibition of ferroptosis in cardiac ischemia/reperfusion (I/R) injury.Journal of translational medicine · 2025Article
- Low doses of ozone alleviate cardiomyocyte ferroptosis induced by hypoxia-reoxygenation injury via the AMPK-mTOR pathway.European journal of medical research · 2025Article
- Remimazolam alleviates myocardial ischemia/reperfusion injury and inflammation via inhibition of the NLRP3/IL‑1β pathway in mice.International journal of molecular medicine · 2025Article
- The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025Review
- Anesthesia-Induced Ferroptosis: Bidirectional Regulation and Molecular Mechanisms in Cardio-Cerebral Injury.Journal of inflammation research · 2025Review
- Ferroptosis in organ ischemia-reperfusion injuries: recent advancements and strategies.Molecular and cellular biochemistry · 2025Review
- Special Issue "New Molecular Insights into Ischemia/Reperfusion".International journal of molecular sciences · 2024Article
- Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury.Cell biochemistry and biophysics · 2024Article
- Propofol Mitigates Sepsis-Induced Brain Injury by Inhibiting Ferroptosis Via Activation of the Nrf2/HO-1axis.Neurochemical research · 2024Article
- Licochalcone A alleviates ferroptosis in doxorubicin-induced cardiotoxicity via the PI3K/AKT/MDM2/p53 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- N-acetylcysteine Protects Against Myocardial Ischemia-Reperfusion Injury Through Anti-ferroptosis in Type 1 Diabetic Mice.Cardiovascular toxicology · 2024Article
- Food therapy of scutellarein ameliorates pirarubicin‑induced cardiotoxicity in rats by inhibiting apoptosis and ferroptosis through regulation of NOX2‑induced oxidative stress.Molecular medicine reports · 2024Article
- Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future.Cell biology and toxicology · 2024Review
- Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury.International journal of molecular sciences · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanism underlying the protective role of propofol against myocardial ischemia/reperfusion (I/R) injury remains poorly understood. Previous studies have shown that ferroptosis is an imperative pathological process in myocardial I/R injury. We hypothesized that propofol prevents myocardial I/R injury by inhibiting ferroptosis via the AKT/p53 signaling pathway. The ferroptosis-inducing agent erastin (E) and AKT inhibitor MK2206 (MK) were used to investigate the role of propofol in myocardial I/R injury. H9C2 cells treated without any reagents, erastin for 24 h, propofol for 1 h before adding erastin were assigned as the control (C), E, and E + P group, respectively. Cell viability, reactive oxygen species (ROS), and the expression of antioxidant enzymes, including ferritin heavy chain 1 (FTH1), cysteine/glutamate transporter (XCT), and glutathione peroxidase 4 (GPX4) in H9C2 cells. Rat hearts from the I/R + P or I/R groups were treated with or without propofol for 20 min before stopping perfusion for 30 min and reperfusion for 60 min. Rat hearts from the I/R + P + MK or I/R + MK groups were treated with or without propofol for 20 min, with a 10-min treatment of MK2206 before stopping perfusion. Myocardial histopathology, mitochondrial structure, iron levels, and antioxidant enzymes expression were assessed. Our results demonstrated that erastin increased H9C2 cell mortality and reduced the expression of antioxidant enzymes. I/R, which reduced the expression of antioxidant enzymes and increased iron or p53 (
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