ArticleInternational journal of nanomedicine2024
Targeted Delivery and ROS-Responsive Release of Lutein Nanoassemblies Inhibit Myocardial Ischemia-Reperfusion Injury by Improving Mitochondrial Function.
Article in International journal of nanomedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Targeted drug delivery systems for cardiovascular disease treatment: principles, targeting strategies, and future prospects.Annals of medicine · 2026Review
- Endogenous and exogenous stimuli-driven intelligent nanocarriers: emerging strategies for the treatment of myocardial infarction.Journal of nanobiotechnology · 2026Review
- Review
- Targeted Delivery of Schisandrin A to Cardiac Endothelium Alleviates Myocardial Ischemia-Reperfusion Injury via Suppression of Ferroptosis.International journal of nanomedicine · 2026Article
- Mechanisms underlying the reversal of hypoxia-induced energy metabolic reprogramming in cardiomyocytes by Poria cocos triterpenoids: integrated regulation of mitochondrial dynamics and the autophagy-lysosomal pathway.Frontiers in cardiovascular medicine · 2026Article
- Engineering the oxidative myocardium: ROS-responsive biomaterials for precision cardiovascular delivery in ischemia-reperfusion injury and post-infarction remodeling.Frontiers in drug delivery · 2026Review
- Mitochondrial dysfunction in immune cells during the perioperative period: mechanisms, emerging therapeutic strategies, and implications for multi-organ protection.Frontiers in immunology · 2026Review
- Redox Signaling Disruption and Antioxidants in Toxicology: From Precision Therapy to Potential Hazards.Cell biochemistry and biophysics · 2025Review
- N-acetylneuraminic acid promotes ferroptosis of H9C2 cardiomyocytes with hypoxia/reoxygenation injury by inhibiting the Nrf2 axis.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Lutein Alleviate Acute Lung Injury Induced by Limb Ischemia-Reperfusion Through PPAR-γ/PI3K/AKT/NLRP3 Signaling.Mediators of inflammation · 2025Article
- Editorial: Novel treatments for cardiovascular diseases by targeting inflammation, oxidative stress, and cell death.Frontiers in cardiovascular medicine · 2024Article
- AlClBioFactors (Oxford, England)Article
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Authors and funding
14 authors.
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Abstract
Purpose: Myocardial ischemia-reperfusion injury (MI/RI) is associated with increased oxidative damage and mitochondrial dysfunction, resulting in an elevated risk of mortality. MI/RI may be alleviated by protecting cardiomyocytes from oxidative stress. Lutein, which belongs to a class of carotenoids, has proven to be effective in cardiovascular disease treatment due to its remarkable antioxidant properties, but its application is limited due to its poor stability and low bioavailability in vivo. Methods: In this study, a delivery system was developed based on distearoyl phosphatidyl ethanolamine (DSPE)-thiol-ketone (TK)-PEG2K (polyethylene glycol 2000) (abbreviated as DTP) and PCM-SH (CWLSEAGPVVTVRALRGTGSW) to deliver lutein (abbreviated as lutein@DTPP) to damaged myocardium. First, lutein, lutein@DTP, or lutein@DTPP were injected through the tail vein once a day for 3 days and then MI/RI model rats were established by exposing rats to ischemia for 45 min and reperfusion for 6 h. We employed a range of experimental techniques including qRT-PCR, Western blotting, transmission electron microscopy, immunohistochemistry, immunofluorescence, flow cytometry, immunoprecipitation, molecular docking, and molecular dynamics simulations. Results: Lutein@DTPP exhibited good myocardial targeting and ROS-responsive release. Our data suggested that lutein@DTPP effectively suppresses ferroptosis in cardiomyocytes. Mechanistically, we observed an upregulation of mouse double minute-2 (MDM2) in the hearts of MI/RI models and cardiomyocytes exposed to hypoxia/reoxygenation (H/R) conditions. In addition, NADH-ubiquinone oxidoreductase 75 kDa Fe-S protein 1 (NDUFS1) translocation from the cytosol to the mitochondria was inhibited by MDM2 upregulation. Notably, no significant variation in the total NDUFS1 expression was observed in H/R-exposed cardiomyocytes following treatment with siMDM2. Further study indicated that lutein facilitates the translocation of NDUFS1 from the cytosol to mitochondria by directly binding and sequestering MDM2, thereby improving mitochondrial function and inhibiting ferroptosis. Conclusion: Lutein@DTPP promoted the mitochondrial translocation of NDUFS1 to restore mitochondrial function and inhibited the ferroptosis of cardiomyocytes by directly binding and sequestering MDM2.
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