The role of foam cells in spinal cord injury: challenges and opportunities for intervention

Frontiers in Immunology, 2024 · DOI: 10.3389/fimmu.2024.1368203 · Published: March 13, 2024

Simple Explanation

Spinal cord injury (SCI) leads to tissue cell debris at the injury site, interacting with cytokines and the central nervous system's glial environment to create an inhibitory microenvironment, hindering nerve regeneration. Macrophages, responsible for removing tissue debris after SCI, can transform into foamy macrophages due to high lipid content and dysregulated lipid metabolism, exacerbating inflammation and impeding nerve repair. This review summarizes macrophage phenotype and metabolism under inflammatory conditions, the mechanisms and consequences of foam cell formation after SCI, and discusses potential therapeutic targets for SCI treatment.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
Foam cells persist in the lesion site after SCI and mediate chronic inflammation, which hampers nerve repair.
2
Macrophages internalize modified lipoproteins via surface scavenger receptors (SRs) like CD36 and SR-A, promoting foam cell formation.
3
Enhancing cholesterol efflux from macrophages in the spinal cord injury site may be a strategy to address foam cell formation and accumulation.

Research Summary

Spinal cord injury results in tissue debris and an inflammatory microenvironment that inhibits nerve regeneration; macrophages, the primary cells for debris removal, can become foam cells, worsening inflammation and hindering repair. The review explores macrophage phenotypes, metabolism, and the mechanisms of foam cell formation after SCI, highlighting the importance of regulating foam cells to promote nerve repair. Two main strategies are proposed: reducing lipid phagocytosis by macrophages and enhancing reverse cholesterol transport mechanisms to prevent foam cell formation and accumulation.

Practical Implications

Targeting Lipid Uptake Receptors

Modulating lipid uptake receptors such as CD36, CD204, and LOX-1 may reduce lipid accumulation in macrophages and subsequent foam cell formation.

Enhancing Reverse Cholesterol Transport

Promoting the reverse cholesterol transport pathway by targeting ApoA-I, ApoE, ABCA1, and ABCG1 can help clear excess lipids from macrophages, preventing foam cell transformation.

Developing ApoE Mimetic Peptides

Exogenous ApoE mimetic peptides show promise as neuroprotective agents capable of crossing the blood-brain barrier and inhibiting foam cell formation after spinal cord injury.

Study Limitations

1
The precise intracellular composition of lipid droplets in foam cells after spinal cord injury requires further analysis.
2
Species-specific variability in cholesterol efflux pathways needs to be considered when designing interventions.
3
The role of non-cholesterol lipids in foam cell formation after spinal cord injury requires more exploration.

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