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Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation

Hongxia Li1,2,3, Zhiqiang Cao1,2,3, Lili Wang1,2,3

  • 1Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Frontiers in Immunology
|April 18, 2022
PubMed

Insights

Atherosclerosis (AS) involves macrophage foam cell formation, influenced by their polarization and death. Understanding these processes, especially ferroptosis, is key for developing targeted therapies for cardiovascular diseases.

Area of Science:

  • Cardiovascular biology
  • Immunology
  • Cellular pathology

Background:

  • Atherosclerosis (AS) is driven by lipid and iron accumulation in arterial plaques, primarily involving macrophages transforming into foam cells.
  • Macrophage phenotypes (M1, M2, M4, Mox, M(Hb), Mhem) and their functions are crucial in AS progression.
  • Macrophage death pathways (apoptosis, necrosis, ferroptosis, autophagy, pyrotopsis) significantly impact plaque development and cardiovascular risk.

Approach:

  • This review summarizes major atherosclerosis hypotheses, identifying common molecular factors.
  • It discusses factors influencing macrophage polarization within the arterial microenvironment.
  • The review examines five types of macrophage death, with a focus on ferroptosis in AS.

Key Points:

  • Macrophage polarization and specific death pathways, particularly ferroptosis, are critical determinants of AS.
  • The interplay between macrophage phenotypes and death mechanisms dictates plaque stability and cardiovascular vulnerability.
  • Targeting macrophage behavior and death is a promising strategy for AS intervention.

Conclusions:

  • A comprehensive understanding of macrophage biology in AS is essential for developing effective therapies.
  • Identifying key molecular targets in macrophage polarization and death can lead to novel treatments for cardiovascular diseases.
  • This review provides insights into cellular and molecular mechanisms for clinical intervention in AS.

Keywords:
atherosclerosis preventioninflammationmacrophage deathmacrophage polarizationplaque formation

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