ArticleBasic research in cardiology2019
Neutrophil proteome shifts over the myocardial infarction time continuum.
Article in Basic research in cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.
- Role of Macrophages in Cardiac Remodeling: Cues From Zebrafish Heart.Immunity, inflammation and disease · 2026Pooled it
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Mechanical Microenvironment in Tumor Immune Evasion: Bidirectional Regulation Between Matrix Stiffness and Immune Cells and Its Therapeutic Implications.International journal of biological sciences · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
- From inflammatory effectors to tissue sculptors: non-canonical functions of neutrophils in repair, barrier remodelling and fibrosis.Frontiers in immunology · 2026Review
- Molecular Mechanisms and Therapeutic Strategies Targeting Cardiac Lymphangiogenesis in Heart Failure.Cardiovascular toxicology · 2025Review
- Targeting a specific subset of neutrophils to mitigate cardiac reperfusion injury.Research square · 2025Article
- The role and therapeutic advances of neutrophils in acute myocardial infarction: from traditional chinese medicine modulation to modern therapeutic strategies.Chinese medicine · 2025Review
- Review
- Ex vivo single-cell profiling of acute myocardial infarction patients reveals disproportionate CD66bBioengineering & translational medicine · 2025Article
- Cardiac ATP production and contractility are favorably regulated by short-term S100A9 blockade after myocardial infarction.Journal of advanced research · 2025Article
- Role of Neutrophils in Homeostasis and Diseases.MedComm · 2025Review
- The cGAS-STING pathway promotes acute ischemia-induced neutropoiesis and neutrophil priming in the bone marrow.Basic research in cardiology · 2025Article
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Complex regulation of cardiac fibrosis: insights from immune cells and signaling pathways.Journal of translational medicine · 2025Review
- Immunological Regulation of Fibrosis During Heart Failure: It Takes Two to Tango.Biomolecules · 2025Review
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
In response to myocardial infarction (MI), neutrophils (PMNs) are early responders that initiate the inflammatory reaction. Because macrophages and fibroblasts show polarization states after MI, we hypothesized PMNs also undergo phenotypic changes over the MI time course. The objective of the current study was to map the continuum of polarization phenotypes in cardiac neutrophils over the first week of MI. C57BL/6J male mice (3-6 months old) underwent permanent coronary artery ligation to induce MI, and PMNs were isolated from the infarct region at days 1, 3, 5, and 7 after MI. Day 0 served as a no MI negative control. Aptamer proteomics was performed on biological replicates (n = 10-12) for each time point. Day (D)1 MI neutrophils had a high degranulation profile with increased matrix metalloproteinase (MMP) activity. D3 MI neutrophil profiles showed upregulation of apoptosis and induction of extracellular matrix (ECM) organization. D5 MI neutrophils further increased their ECM reorganization profile. D7 MI neutrophils had a reparative signature that included expression of fibronectin, galectin-3, and fibrinogen to contribute to scar formation by stimulating ECM reorganization. Of note, fibronectin was a key modulator of degranulation, as it amplified MMP-9 release in the presence of an inflammatory stimulus. Our results indicate that neutrophils selectively degranulate over the MI time course, reflective of both their intrinsic protein profiles as well as the ECM environment in which they reside. MMPs, cathepsins, and ECM proteins were prominent neutrophil degranulation indicators.
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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.