Key result
Neutrophils play a complex role in cardiac wound healing after myocardial infarction by shifting from a pro-inflammatory to a reparative phenotype and communicating with cardiomyocytes and macrophages.
Why the study?
Neutrophils paradoxically impair myocardial infarction resolution when increased or depleted, reflecting a complex role and shifts in phenotype during cardiac wound healing.
This review highlights the complex, biphasic role of neutrophils in post-MI cardiac wound healing and their crosstalk with other cardiac cells.
Answers are grounded in this paper and cite their sources.
Both neutrophil excess and depletion impair post-MI repair; challenges broad anti-inflammatory strategies and extends biphasic immune-response models.
Myocardial infarction (MI) initiates an intense inflammatory response that induces neutrophil infiltration into the infarct region. Neutrophils commence the pro-inflammatory response that includes upregulation of cytokines and chemokines (e.g., interleukin-1 beta) and degranulation of pre-formed proteases (e.g., matrix metalloproteinases -8 and -9) that degrade existing extracellular matrix to clear necrotic tissue. An increase or complete depletion of neutrophils both paradoxically impair MI resolution, indicating a complex role of neutrophils in cardiac wound healing. Following pro-inflammation, the neutrophil shifts to a reparative phenotype that promotes inflammation resolution and aids in scar formation. Across the shifts in phenotype, the neutrophil communicates with other cells to coordinate repair and scar formation. This review summarizes our current understanding of neutrophil crosstalk with cardiomyocytes and macrophages during MI wound healing.
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Chalise et al. (2021) conducted a review in Myocardial infarction. Neutrophil crosstalk was evaluated. Neutrophils play a complex role in cardiac wound healing after myocardial infarction by shifting from a pro-inflammatory to a reparative phenotype and communicating with cardiomyocytes and macrophages.
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