ReviewJournal of innate immunity2026
Neutrophil Heterogeneity after Myocardial Infarction.
Review in Journal of innate immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
3 authors.
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Abstract
backgroundCardiovascular diseases (CVDs), including myocardial infarction (MI), are the leading cause of death worldwide. Neutrophils have emerged as actors in noninfectious pathologies and play major roles in CVDs: after MI, neutrophils are the first cell recruited to the ischemic heart and display multifaceted roles in orchestrating post-MI tissue healing and repair. Interestingly, recent studies described a high heterogeneity in neutrophils during this process. SUMMARY: At steady state, neutrophils present diversity during their development in hematopoietic organs and in the circulation after reaching maturity. Inflammatory environments elicit neutrophil reprogramming and further complexify neutrophil heterogeneity, especially leading to the emergence of tissue-specific populations including SiglecF+ neutrophils. Neutrophils play beneficial and deleterious roles after MI: they originate from diverse sources including the bone marrow, the spleen, and from the marginated neutrophil pool and display a time-dependent appearance of heterogeneous profile within the cardiac tissue. KEY MESSAGES: Neutrophil heterogeneity in the cardiac tissue could explain the contrasting roles ascribed to neutrophils after MI. Increased knowledge in neutrophil diversity will enable the identification of specific targets to improve cardiac healing processes.
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