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What are the cellular impact of a myocardial infarction ? 


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Following a myocardial infarction (MI), various cellular impacts are observed. The repair process post-MI involves three overlapping phases: the inflammatory phase, proliferative phase, and maturation phase, where immune cells like macrophages, neutrophils, and lymphocytes play crucial roles in governing these phases . Additionally, studies highlight the emergence of different cellular phenotypes in the infarcted heart, such as senescent cells, inflammatory cells, and dedifferentiated cardiomyocytes, which contribute to adverse remodeling and impaired healing post-MI . Single-cell RNA sequencing data in murine hearts post-MI revealed immune cell heterogeneity, with distinct proinflammatory and prophagocytic capabilities in macrophages, and sequential cell-fate transitions in neutrophils, indicating complex transcriptional profiles and pathways post-MI . Understanding these cellular impacts is crucial for developing targeted therapies to prevent heart failure after MI.

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The impact of a myocardial infarction includes temporal changes in immune cell functions, involving macrophages, neutrophils, and lymphocytes, influencing cardiac repair and potential heart failure development.
Myocardial infarction leads to immune cell infiltration, with distinct macrophage subsets showing proinflammatory or prophagocytic capabilities, and neutrophils exhibiting sequential activation states in the ischemic heart.
The paper discusses the impact of myocardial infarction on immune cell dynamics, specifically macrophages, neutrophils, and lymphocytes, during the repair process.
The paper discusses the cellular phenotypes and pathways implicated in injury, remodeling, and regeneration of the myocardium after myocardial infarction.

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