ArticleiScience2025
Active and passive targeted delivery of anti-ferroptotic therapy for post-resuscitation myocardial dysfunction.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.CNS neuroscience & therapeutics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-resuscitation myocardial dysfunction (PRMD), associated with ferroptosis, contributes significantly to early mortality post-cardiopulmonary resuscitation. However, ferrostatin-1 (Fer-1), a ferroptosis inhibitor, faces challenges in clinical applicability for critical diseases. Here, we report a reactive oxygen species (ROS)-responsive (passively targeting ferroptosis) and myocardium-targeted drug delivery system that facilitates the on-demand delivery of nanoparticles (NPs) encapsulating a ferroptotic inhibitor as tested in a cardiac arrest model. Compared to ROSR@Fer-1 and free drugs, APTD@Fer-1 NPs exhibited good biocompatibility and significantly inhibited hypoxia-reoxygenation-induced ferroptosis in H9c2 cells. In rats, APTD @Fer-1 NPs improved PRMD, oxidative stress, inflammatory response, cardiac remodeling, and subsequent survival prognosis by inhibiting myocardial ferroptosis at 6 and 72 h after resuscitation. Importantly, APTD@Fer-1NPs allow for intravenous injections, emergency treatment, and single administration, offering a drug delivery strategy appropriate for critical care settings. These results offer insights that will facilitate further exploration of precision treatments for PRMD.
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Registered trials
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.