Cellular mechanisms underlying the impairment of macrophage efferocytosis

Yonggang Ma1, Scott S Kemp1, Xiaoyuan Yang1

  • 1Department of Molecular Pharmacology and Physiology, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA.

Immunology Letters
|February 5, 2023
PubMed

Insights

Efficient clearance of dying cells by macrophages, known as efferocytosis, is vital for tissue repair and preventing inflammation. Defects in this process contribute to various diseases, highlighting potential therapeutic targets.

Area of Science:

  • Immunology
  • Cell Biology
  • Pathology

Background:

  • Efferocytosis, the clearance of dying cells by macrophages, is crucial for tissue homeostasis and repair.
  • Failure in timely efferocytosis can lead to secondary necrosis, inflammation, and autoimmune responses.
  • Defects in macrophage efferocytosis are implicated in numerous inflammatory and autoimmune diseases.

Purpose of the Study:

  • To review the normal processes and importance of macrophage efferocytosis.
  • To analyze the molecular mechanisms of efferocytosis impairment in disease.
  • To discuss potential therapeutic targets for enhancing efferocytosis.

Main Methods:

  • Literature review of current knowledge on efferocytosis.
  • Analysis of signaling and metabolic pathways involved in efferocytosis.
  • Examination of molecular and cellular mechanisms of efferocytosis defects.

Main Results:

  • Efferocytosis is essential for initiating tissue repair through pro-reparative factors.
  • Complex and incompletely understood mechanisms underlie efferocytosis impairment in disease.
  • Potential molecular targets for enhancing efferocytosis in disease models have been identified.

Conclusions:

  • Dysfunctional efferocytosis contributes significantly to inflammatory and autoimmune diseases.
  • Targeting efferocytosis pathways offers potential therapeutic strategies for various conditions.
  • Understanding efferocytosis mechanisms is key to developing novel treatments for related diseases.