ArticleBioengineered2022
Propofol protects cardiomyocytes from doxorubicin-induced toxic injury by activating the nuclear factor erythroid 2-related factor 2/glutathione peroxidase 4 signaling pathways.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Propofol in combination with salvianolic acid A protect against lipopolysaccharide-induced cardiac dysfunction and ferroptosis through activating the SIRT1/FoxO1 signaling under diabetic condition.Annals of medicine · 2025Article
- AICAr Inhibition of cardiomyocyte autophagy promotes p62-dependent NRF2 expression and protection against doxorubicin toxicity.Cellular and molecular life sciences : CMLS · 2025Article
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Ciprofol prevents ferroptosis in LPS induced acute lung injury by activating the Nrf2 signaling pathway.BMC pulmonary medicine · 2024Article
- Molecular Mechanisms and Therapeutic Targeting of Ferroptosis in Doxorubicin-Induced Cardiotoxicity.JACC. Basic to translational science · 2024Review
- Nicotinamide ribose ameliorates myocardial ischemia/reperfusion injury by regulating autophagy and regulating oxidative stress.Experimental and therapeutic medicine · 2024Article
- Protective Role of Dioscin against Doxorubicin-Induced Chronic Cardiotoxicity: Insights from Nrf2-GPX4 Axis-Mediated Cardiac Ferroptosis.Biomolecules · 2024Article
- 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
- Ferroptosis inhibitor alleviates sorafenib-induced cardiotoxicity by attenuating KLF11-mediated FSP1-dependent ferroptosis.International journal of biological sciences · 2024Article
- Ciprofol Ameliorates Myocardial Ischemia/Reperfusion Injury by Inhibiting Ferroptosis Through Upregulating HIF-1α.Drug design, development and therapy · 2024Article
- Role of ferroptosis in effects of anesthetics on multiple organ diseases: A literature review.Heliyon · 2023Review
- Broadening horizons: The role of ferroptosis in myocardial ischemia-reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Nrf2: a dark horse in doxorubicin-induced cardiotoxicity.Cell death discovery · 2023Review
- The dual role of ferroptosis in anthracycline-based chemotherapy includes reducing resistance and increasing toxicity.Cell death discovery · 2023Review
- Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy.Experimental and therapeutic medicine · 2023Article
- Galangin Attenuates Myocardial Ischemic Reperfusion-Induced Ferroptosis by Targeting Nrf2/Gpx4 Signaling Pathway.Drug design, development and therapy · 2023Article
- Sitagliptin mitigates hypoxia/reoxygenation (H/R)-induced injury in cardiomyocytes by mediating sirtuin 3 (SIRT3) and autophagy.Bioengineered · 2022Article
- Relevance of Ferroptosis to Cardiotoxicity Caused by Anthracyclines: Mechanisms to Target Treatments.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Propofol offers important protective effects in ischemia/reperfusion-induced cardiomyocyte injury, but its specific mechanisms in doxorubicin (DOX)-induced cardiotoxicity have not been investigated. In this paper, we attempted to explore the effects of propofol on DOX-induced human cardiomyocyte injury and its related mechanisms. H9c2 cell viability was assessed by cell counting kit-8 and lactate dehydrogenase assay kit. Nuclear factor erythroid 2-related factor 2 (NRF2)/glutathione peroxidase 4 (GPx4) signaling pathway-related protein levels were measured by Western blot. Ferroptosis was evaluated by corresponding kits and Western blot and apoptosis was detected by CCK-8, terminal deoxynucleotidyl transferase dUTP nick-end labeling and Western blot. Oxidative stress was assessed by reactive oxygen species kit and the commercial kits, and inflammation response was analyzed by enzyme-linked immunosorbent assay and Western blot. The results showed that propofol attenuated DOX-induced cytotoxicity and activated Nrf2/GPx4 signaling pathways in H9c2 cells. In addition, propofol also alleviated DOX-induced ferroptosis, increased cell viability and inhibited apoptosis, oxidative stress and inflammatory responses in H9c2 cells through activation of Nrf2/GPx4 signaling pathways. In summary, propofol provides the protection against DOX-induced cardiomyocyte injury by activating Nrf2/GPx4 signaling, providing a new approach and theoretical basis for the repair of cardiomyocytes.
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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.