ArticleNature communications2024
Spatiotemporal control of neutrophil fate to tune inflammation and repair for myocardial infarction therapy.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
43 citing papers in PubMed.
- Remote electroacupuncture conditioning protects the heart via fine-tuning the dual role of the SDF-1α/CXCR4 axis in myocardial ischemia-reperfusion injury.Chinese medicine · 2026Article
- Immature neutrophils sound the alarm in acute myocardial infarction.Nature cardiovascular research · 2026Article
- CD34Histology and histopathology · 2026Review
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Cardiac regeneration and repair: the emerging mechanisms and therapeutic approaches.Molecular biomedicine · 2026Review
- Inflammation-Mediated Mechanisms of Arrhythmias After Acute Myocardial Infarction.Reviews in cardiovascular medicine · 2026Review
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Artificial exosomes synergistically reshape sepsis immune homeostasis by modulating neutrophil fate and blocking PD-1/PD-L1.Cell reports. Medicine · 2026Article
- Interleukin enhancer binding factor 3 exacerbates cardiac inflammation and injury following myocardial infarction by inhibiting Lys48-linked ubiquitination on HNRNPA2B1 in macrophages.Cellular & molecular immunology · 2026Article
- ROS-responsive hydrogel patch orchestrating macrophage reprogramming and mitochondrial protection for post-MI repair.Bioactive materials · 2026Article
- A robust adhesive microneedle for oral infections therapy via synergistic antibacterial and neutrophil-macrophage axis immunomodulation.Science advances · 2026Article
- [Mechanisms of Macrophage Efferocytosis-driven Remodeling of Lung Cancer Microenvironment Structure and Angiogenesis and Prospects for Clinical Intervention].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- A call to redefine cardiovascular immunobiology around leukocyte plasticity.American journal of physiology. Heart and circulatory physiology · 2026Article
- Myocardial Ischemia-Reperfusion Injury-Mechanistic Insights and Novel Therapeutics.International journal of molecular sciences · 2026Review
- Endogenous and exogenous stimuli-driven intelligent nanocarriers: emerging strategies for the treatment of myocardial infarction.Journal of nanobiotechnology · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Dynamic Regulation of Collagens, Proteases, Their Inhibitors, and Cell Death in Experimental Asthma in Mice.Allergy · 2026Article
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Emerging insights of bile acids in cardiovascular physiology and disease: from molecular mechanisms to therapeutic potential.Frontiers in pharmacology · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are critical mediators of both the initiation and resolution of inflammation after myocardial infarction (MI). Overexuberant neutrophil signaling after MI exacerbates cardiomyocyte apoptosis and cardiac remodeling while neutrophil apoptosis at the injury site promotes macrophage polarization toward a pro-resolving phenotype. Here, we describe a nanoparticle that provides spatiotemporal control over neutrophil fate to both stymie MI pathogenesis and promote healing. Intravenous injection of roscovitine/catalase-loaded poly(lactic-co-glycolic acid) nanoparticles after MI leads to nanoparticle uptake by circulating neutrophils migrating to the infarcted heart. Activated neutrophils at the infarcted heart generate reactive oxygen species, triggering intracellular release of roscovitine, a cyclin-dependent kinase inhibitor, from the nanoparticles, thereby inducing neutrophil apoptosis. Timely apoptosis of activated neutrophils at the infarcted heart limits neutrophil-driven inflammation, promotes macrophage polarization toward a pro-resolving phenotype, and preserves heart function. Modulating neutrophil fate to tune both inflammatory and reparatory processes may be an effective strategy to treat MI.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.