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Mechanisms of continual efferocytosis by macrophages and its role in mitigating atherosclerosis

Dhananjay Kumar1, Rajan Pandit1, Arif Yurdagul1

  • 1Molecular and Cellular Physiology, Louisiana State University Health Sciences Center at Shreveport, Shreveport, LA, USA.

Immunometabolism (Cobham, Surrey)
|January 30, 2023
PubMed

Insights

Impaired efferocytosis, the clearance of dead cells, worsens atherosclerosis by forming necrotic cores. Enhancing continual efferocytosis may resolve inflammation and improve plaque stability.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cellular Metabolism

Background:

  • Atherosclerotic cardiovascular disease is a leading global cause of mortality.
  • Plaque vulnerability is linked to necrotic core expansion and thin fibrous caps.
  • Impaired efferocytosis (clearance of apoptotic cells) contributes to plaque instability in chronic inflammatory diseases like atherosclerosis.

Purpose of the Study:

  • To review the mechanisms of continual efferocytosis and its role in atherosclerosis.
  • To explore how dysregulation of continual efferocytosis leads to nonresolving inflammation.
  • To discuss potential strategies for enhancing efferocytosis in disease.

Main Methods:

  • Review of current literature on efferocytosis and atherosclerosis.
  • Analysis of cellular and molecular mechanisms of continual efferocytosis.
  • Discussion of in vivo findings related to efferocytosis defects.

Main Results:

  • Continual efferocytosis is distinct from single efferocytosis and crucial for handling apoptotic cell cargo.
  • Defects in continual efferocytosis lead to secondary necrosis, inflammation, and worsened atherosclerosis.
  • Dysregulation of efferocytosis contributes to nonresolving inflammation in atherosclerotic plaques.

Conclusions:

  • Understanding continual efferocytosis is key to addressing plaque vulnerability.
  • Targeting efferocytosis pathways may offer therapeutic strategies for atherosclerosis.
  • Enhancing efferocytosis could resolve inflammation and promote plaque stabilization.

Keywords:
atherosclerosisefferocytosismacrophages

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