ReviewArteriosclerosis, thrombosis, and vascular biology2026
Macrophages and the Survival of Cardiomyocytes After Myocardial Infarction.
Review in Arteriosclerosis, thrombosis, and vascular biology, 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
2 authors.
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Abstract
Myocardial infarction (MI) causes a severe burden to public health worldwide. After MI, stressed cardiomyocytes undergo necrosis and regulated cell death. Dynamic cell cascades ensue to limit tissue injury and promote healing. MI and subsequent ischemic injury trigger the influx of innate immune cells. Macrophages, among the first responders of MI, are known mostly to coordinate the scavenging of dead cardiomyocytes. However, rather than occurring as a homogenous population, macrophages have diverse ontogenies and pathological functions, exhibiting contradictory roles in the survival and death of cardiomyocytes. This review focused on macrophages and discussed their diverse dynamics and functional patterns after MI. We shared the insight into the roles of macrophages in cardiomyocyte survival and regulated cell death. We explored the use of single-cell technology to discriminate specific macrophage clusters that can provide clues for the precise targeting of cardiomyocyte survival after MI.
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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 Socratic graph.