ArticleACS omega2025
Ultrasound-Triggering Carbon Monoxide Release from Rhodium Nanoparticles for Myocardial Infarction Treatment.
Article in ACS omega, 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.
- Controlled Delivery of Gasotransmitters for Cardiovascular Therapy: Molecular Mechanisms, Engineered Platforms, and Translational Perspectives.International journal of nanomedicine · 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ST-segment elevation myocardial infarction (STEMI) represents the most severe clinical manifestation of coronary heart disease. Despite the availability of current treatments, their high cost and surgical complexity have limited their effectiveness in reducing the associated high rates of disability and mortality. Additionally, conventional nanoparticles face significant challenges in achieving precise and controlled drug release within the infarcted myocardium. In this study, we developed a carbon monoxide (CO)-releasing system based on rhodium nanodots. The resulting nanoparticles (Rh-PEG-CO NDs) enable site-specific CO release from infarcted cardiac tissue upon ultrasound stimulation. The combination of CO and rhodium nanodots effectively scavenges reactive oxygen species (ROS) and mitigates postinfarction myocardial fibrosis, thereby attenuating the inflammatory response in the infarcted region. Both in vitro and in vivo experiments demonstrated that these functional nanoparticles exhibit high efficacy in inhibiting cardiomyocyte apoptosis, reversing pathological cardiac remodeling, and improving overall cardiac function. This study presents a novel CO-releasing platform that advances the clinical potential of CO-based therapies and underscores the promise of metal-based nanomaterials in biomedical applications.
Identifiers
What Socratic holds
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 Socratic graph.