Phagocyte-myocyte interactions and consequences during hypoxic wound healing

Shuang Zhang, Shirley Dehn, Matthew DeBerge, Ki Jong Rhee, Barry Hudson, Edward B. Thorp*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Myocardial infarction (MI), secondary to atherosclerotic plaque rupture and occlusive thrombi, triggers acute margination of inflammatory neutrophils and monocyte phagocyte subsets to the damaged heart, the latter of which may give rise briefly to differentiated macrophage-like or dendritic-like cells. Within the injured myocardium, a primary function of these phagocytic cells is to remove damaged extracellular matrix, necrotic and apoptotic cardiac cells, as well as immune cells that turn over. Recognition of dying cellular targets by phagocytes triggers intracellular signaling, particularly in macrophages, wherein cytokines and lipid mediators are generated to promote inflammation resolution, fibrotic scarring, angiogenesis, and compensatory organ remodeling. These actions cooperate in an effort to preserve myocardial contractility and prevent heart failure. Immune cell function is modulated by local tissue factors that include secreted protease activity, oxidative stress during clinical reperfusion, and hypoxia. Importantly, experimental evidence suggests that monocyte function and phagocytosis efficiency is compromised in the setting of MI risk factors, including hyperlipidemia and ageing, however underlying mechanisms remain unclear. Herein we review seminal phagocyte and cardiac molecular factors that lead to, and culminate in, the recognition and removal of dying injured myocardium, the effects of hypoxia, and their relationship to cardiac infarct size and heart healing.

Original languageEnglish (US)
Pages (from-to)65-73
Number of pages9
JournalCellular Immunology
Issue number1-2
StatePublished - Sep 1 2014


  • Cardiomyocyte
  • Monocyte
  • Myocardial infarction

ASJC Scopus subject areas

  • Immunology


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