Neutrophil crosstalk during cardiac wound healing after myocardial infarction

Upendra Chalise, Mediha Becirovic-Agic, Merry L. Lindsey

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations


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 matrix metalloproteinases-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.

Original languageEnglish (US)
Article number100485
JournalCurrent Opinion in Physiology
StatePublished - Dec 2021

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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