ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Injured Myocardium-Targeted Theranostic Nanoplatform for Multi-Dimensional Immune-Inflammation Regulation in Acute Myocardial Infarction.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed.
- 4-Octyl Itaconate Attenuates Age-Induced Parotid Gland Dysfunction Through the Suppression of Fibrosis and Lipid Deposition by AMPKα/PPARα and the Inhibition of Oxidative Stress via the AMPKα/Nrf2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Nanomedicine in Cardiovascular Inflammation: Novel Diagnostic and Therapeutic Strategies.Journal of personalized medicine · 2026Review
- SLC7A11-mediated cystine accumulation and Rac1-WRC-Arp2/3-driven actin cytoskeletal folding synergistically induce disulfidptosis in acute myocardial infarction.Communications biology · 2026Article
- A spatiotemporally coordinated curcumin-based microneedle patch for SDF-1α delivery and synergistic myocardial infarction therapy.Journal of nanobiotechnology · 2026Article
- Neutrophil-based delivery platforms: from natural mechanisms to engineered therapeutics.Theranostics · 2026Review
- Positron Emission Tomography/Computed Tomography Imaging-Guided Polydopamine Nanoparticles Attenuate Foam Cell Ferroptosis for Targeted Antiatherosclerotic Therapy.Small science · 2025Article
- Engineered hybrid cell membrane nanosystems for treating cardiovascular diseases.Materials today. Bio · 2025Review
- Injured Myocardium-Targeted Theranostic Nanoplatform for Multi-Dimensional Immune-Inflammation Regulation in Acute Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Advanced Nanomaterial Platforms for Targeted Therapy of Myocardial Ischemia-Reperfusion Injury.Research (Washington, D.C.) · 2025Review
- Biomimetic Brain-Targeted Drug Delivery System for the Treatment of Brain Diseases.Current drug delivery · 2025Review
- Macrophage polarization in acute myocardial infarction: multidimensional regulation and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Pyroptosis is a key mode of programmed cell death during the early stages following acute myocardial infarction (AMI), driving immune-inflammatory responses. Cardiac resident macrophages (CRMs) are the primary mediators of cardiac immunity, and they serve a dual role through their shaping of both myocardial injury and post-AMI myocardial repair. To appropriately regulate AMI-associated inflammation, HM4oRL is herein designed, an innovative bifunctional therapeutic nanoplatform capable of inhibiting cardiomyocyte pyroptosis while reprogramming inflammatory signaling. This HM4oRL platform is composed of a core of 4-Octyl itaconate (4-OI)-loaded liposomes, a middle layer consisting of a metal-polyphenol network (MPN) film, and an optimized outer hybrid immune-cell membrane layer. The unique properties of this hybrid membrane layer facilitated HM4oRL targeting to the injured myocardium during early-stage AMI in mice, whereupon the release of 4-Ol and modified MPN synergistically inhibited cardiomyocyte pyroptosis while suppressing inflammatory monocytes/macrophage responses at the infarcted site. Mechanistically, HM4oRL preserved cardiac metabolic homeostasis through AMPK signaling activation, establishing favorable microenvironmental conditions for the reprogramming of CRM-mediated inflammation. Ultimately, HM4oRL treatment is able to resolve inflammation, enhance neovascularization, and suppress myocardial fibrosis, reducing the infarct size and enhancing post-AMI cardiac repair such that it is an innovative approach to the targeted treatment of AMI.
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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.