ArticleJournal of advanced research2024
Sulfide-modified nanoscale zero-valent iron as a novel therapeutic remedy for septic myocardial injury.
Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Endogenous H₂S promotes HSPA8 sulfhydration to downregulate HIF1α and prevent ferroptosis in septic myocardial injury.Redox report : communications in free radical research · 2026Article
- Exploration and prospect of core research hotspots in sepsis-induced myocardial injury based on bibliometrics.Medicine · 2026Article
- Signaling Pathways (TNF-α-NF-κB, TLR2-TLR4 as well as ROS-MDA) and Cardiac Damages during Cardiac Surgeries (Coronary Stenting, Permanent Pacemaker Implantations, Radiofrequency Ablations).Current topics in medicinal chemistry · 2025Article
- Nanozymes Targeting Redox Imbalance: A Novel Weapon for Immunomodulation and Organ Protection in Sepsis.International journal of nanomedicine · 2025Review
- How Extracellular Nano-Vesicles Can Play a Role in Sepsis? An Evidence-Based Review of the Literature.International journal of nanomedicine · 2023Review
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Authors and funding
13 authors.
Funding
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Abstract
introductionMyocardial injury is a serious complication in sepsis with high mortality. Zero-valent iron nanoparticles (nanoFe) displayed novel roles in cecal ligation and puncture (CLP)-induced septic mouse model. Nonetheless, its high reactivity makes it difficult for long-term storage.
objectivesTo overcome the obstacle and improve therapeutic efficiency, a surface passivation of nanoFe was designed using sodium sulfide.
methodsWe prepared iron sulfide nanoclusters and constructed CLP mouse models. Then the effect of sulfide-modified nanoscale zero-valent iron (S-nanoFe) on the survival rate, blood routine parameters, blood biochemical parameters, cardiac function, and pathological indicators of myocardium was observed. RNA-seq was used to further explore the comprehensive protective mechanisms of S-nanoFe. Finally, the stability of S-nanoFe-1d and S-nanoFe-30 d, together with the therapeutic efficacy of sepsis between S-nanoFe and nanoFe was compared.
resultsThe results revealed that S-nanoFe significantly inhibited the growth of bacteria and exerted a protective role against septic myocardial injury. S-nanoFe treatment activated AMPK signaling and ameliorated several CLP-induced pathological processes including myocardial inflammation, oxidative stress, mitochondrial dysfunction. RNA-seq analysis further clarified the comprehensive myocardial protective mechanisms of S-nanoFe against septic injury. Importantly, S-nanoFe had a good stability and a comparable protective efficacy to nanoFe.
conclusionsThe surface vulcanization strategy for nanoFe has a significant protective role against sepsis and septic myocardial injury. This study provides an alternative strategy for overcoming sepsis and septic myocardial injury and opens up possibilities for the development of nanoparticle in infectious diseases.
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