Mechanisms and consequences of efferocytosis in advanced atherosclerosis

Edward Thorp, Ira Tabas*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

165 Scopus citations


Throughout atherosclerotic lesion development, intimal macrophages undergo apoptosis, a form of death that usually prevents cellular necrosis. In advanced atherosclerotic lesions, however, these apoptotic macrophages become secondarily necrotic and coalesce over time into a key feature of vulnerable plaques, the necrotic core. This event is critically important, as necrotic core formation in these advanced atheromata is thought to promote plaque disruption and ultimately, acute atherothrombotic vascular disease. Increasing evidence suggests that the mechanism behind postapoptotic macrophage necrosis in advanced atherosclerosis is defective phagocytic clearance or "efferocytosis" of the apoptotic cells. Thus, understanding the cellular and molecular mechanisms of efferocytosis in atherosclerosis and why efferocytosis becomes defective in advanced lesions is an important goal. Molecular-genetic causation studies in mouse models of advanced atherosclerosis have provided evidence that several molecules known to be involved in efferocytosis, including TG2, MFG-E8, complement C1q, Mertk, lysoPC, and Fas, play important roles in the clearance of apoptotic cells in advanced plaques. These and future insights into the molecular mechanisms of defective efferocytosis in advanced atheromata may open the way for novel therapeutic strategies for atherothrombotic vascular disease, the leading cause of death in the industrialized world.

Original languageEnglish (US)
Pages (from-to)1089-1095
Number of pages7
JournalJournal of Leukocyte Biology
Issue number5
StatePublished - Nov 2009

ASJC Scopus subject areas

  • Immunology and Allergy
  • Cell Biology
  • Immunology


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