Immune regulation of cardiac fibrosis post myocardial infarction

Yusra Zaidi, Eslie G. Aguilar, Miguel Troncoso, Daria V. Ilatovskaya, Kristine Y. DeLeon-Pennell

Research output: Contribution to journalReview articlepeer-review

27 Scopus citations


Pathological changes resulting from myocardial infarction (MI) include extracellular matrix alterations of the left ventricle, which can lead to cardiac stiffness and impair systolic and diastolic function. The signals released from necrotic tissue initiate the immune cascade, triggering an extensive inflammatory response followed by reparative fibrosis of the infarct area. Immune cells such as neutrophils, monocytes, macrophages, mast cells, T-cells, and dendritic cells play distinct roles in orchestrating this complex pathological condition, and regulate the balance between pro-fibrotic and anti-fibrotic responses. This review discusses how molecular signals between fibroblasts and immune cells mutually regulate fibrosis post-MI, and outlines the emerging pharmacological targets and therapies for modulating inflammation and cardiac fibrosis associated with MI.

Original languageEnglish (US)
Article number109837
JournalCellular Signalling
StatePublished - Jan 2021


  • Fibrosis
  • Heart failure
  • Inflammation
  • Leukocytes
  • Myocardial infarction
  • T-cells

ASJC Scopus subject areas

  • Cell Biology


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