ArticleFrontiers in pharmacology2022
HJ11 decoction restrains development of myocardial ischemia-reperfusion injury in rats by suppressing ACSL4-mediated ferroptosis.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 26 citations in OpenAlex.
- Synergistic cardioprotection by liraglutide and deferoxamine against doxorubicin-induced cardiotoxicity via modulation of ACSL-4/Nrf-2/GPX-4 signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Traditional Chinese Herbal Formula XuMingZhuSan Alleviates Neuronal Ferroptosis in Rats After Stroke by Activating the NRF2/GPX4/SLC7A11 Pathway.Food science & nutrition · 2026Article
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- Hypoxia Aggravates Myocardial Ischemia/Reperfusion Injury Through the Promotion of Ferroptosis via ACSL4 Lactylation.Journal of cardiovascular translational research · 2025Article
- Exploration of the Potential Bioactive Compounds and Functional Mechanism of Chaihu Sanshen Capsule in Ameliorating Myocardial Ischaemia-Reperfusion Injury: A Serum Pharmaco-Chemistry With Network Pharmacology Analysis.Journal of cellular and molecular medicine · 2025Article
- Melatonin inhibits ferroptosis through the ATF3/GPX4 signaling pathway to relieve myocardial ischemia-reperfusion injury in rats.In vitro cellular & developmental biology. Animal · 2025Article
- Chinese Medicine Formula HJ11 Alleviates Atherosclerosis by Inactivating the TLR4/MyD88/IκB-α Pathway and Modulating the Heart-Gut Axis Response.Journal of inflammation research · 2025Article
- Mechanism of HJ11 Decoction in the Treatment of Atherosclerosis Based on Network Pharmacology and Experimental Validation.Combinatorial chemistry & high throughput screening · 2025Article
- Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.American journal of cardiovascular disease · 2025Review
- Iron promotes both ferroptosis and necroptosis in the early stage of reperfusion in ischemic stroke.Genes & diseases · 2024Article
- LncRNA RNA ROR Aggravates Hypoxia/Reoxygenation-Induced Cardiomyocyte Ferroptosis by Targeting miR-769-5p/CBX7 Axis.Biochemical genetics · 2024Article
- Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3-mediated mitochondrial autophagy.CNS neuroscience & therapeutics · 2024Article
- ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling.Experimental and therapeutic medicine · 2024Article
- Ferroptosis and myocardial ischemia-reperfusion: mechanistic insights and new therapeutic perspectives.Frontiers in pharmacology · 2024Review
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
- The mechanisms crosstalk and therapeutic opportunities between ferroptosis and ovary diseases.Frontiers in endocrinology · 2023Review
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Authors and funding
9 authors at 5 institutions in 1 country.
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Abstract
HJ11 is a novel traditional Chinese medicine developed from the appropriate addition and reduction of Si-Miao-Yong-An decoction, which has been commonly used to treat ischemia-reperfusion (I/R) injury in the clinical setting. However, the mechanism of action of HJ11 components remains unclear. Ferroptosis is a critical factor that promotes myocardial I/R injury, and the pathophysiological ferroptosis-mediated lipid peroxidation causes I/R injury. Therefore, this study explored whether HJ11 decoction ameliorates myocardial I/R injury by attenuating ACSL4-mediated ferroptosis. This study also explored the effect of ACSL4 expression on iron-dependent programmed cell death by preparing a rat model of myocardial I/R injury and oxygen glucose deprivation/reperfusion (OGD/R)-induced H9c2 cells. The results showed that HJ11 decoction improved cardiac function; attenuated I/R injury, apoptosis, oxidative stress, mitochondrial damage, and iron accumulation; and reduced infarct size in the myocardial I/R injury rat model. Additionally, HJ11 decoction suppressed the expression of ferroptosis-promoting proteins [Acyl-CoA synthetase long-chain family member 4 (ACSL4) and cyclooxygenase-2 (COX2)] but promoted the expression of ferroptosis-inhibiting proteins [ferritin heavy chain 1 (FTH1) and glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4)] in the myocardial tissues of the I/R injury rat model. Similar results were found with the OGD/R-induced H9c2 cells. Interestingly, ACSL4 knockdown attenuated iron accumulation, oxidative stress, and ferroptosis in the OGD/R-treated H9c2 cells. However, ACSL4 overexpression counteracted the inhibitory effect of the HJ11 decoction on OGD/R-triggered oxidative stress and ferroptosis in H9c2 cells. These findings suggest that HJ11 decoction restrained the development of myocardial I/R injury by regulating ACSL4-mediated ferroptosis. Thus, HJ11 decoction may be an effective medication to treat myocardial I/R injury.
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