ArticleCommunications biology2025
Lipid accumulation in foam cells drives C1q-dependent synaptic loss and impairs motor function recovery after spinal cord injury.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Broad-Coverage Lipidomics Reveals Temporal Lipid Remodeling and Candidate Serum Biomarkers After Acute Spinal Cord Injury in Rats.Biomedicines · 2026Article
- IL-33/ST2 Signaling and Microglial Functional-State Transitions After Spinal Cord Injury: Direct Evidence and Mechanistic Hypotheses.International journal of molecular sciences · 2026Review
- Activation of the Reverse Cholesterol Transport Pathway: A Strategy to Ameliorate Lipid Metabolic Dyshomeostasis in the Microenvironment Following Spinal Cord Injury.Cellular and molecular neurobiology · 2026Article
- Single-cell analysis reveals an endothelial TP53-CXCL14 axis in breast cancer progression.Journal of translational medicine · 2026Article
- Lysosomes as chemical and metabolic organizers of central nervous system injury and repair.Frontiers in chemistry · 2026Review
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Authors and funding
12 authors.
Funding
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Abstract
Macrophages play a critical role in the repair process following spinal cord injury (SCI), yet the complex mechanisms underlying their functionality remain poorly understood. Using single-cell RNA sequencing, we identified distinct macrophage subpopulations post-SCI, with lipid-laden macrophages, or foam cells, representing the terminal differentiation stage and persisting throughout the chronic phase. Our findings reveal that foam cells display increased expression of C1q, a complement component, which thereby activates microglial phagocytosis of synapses adjacent to the lesion site. This process results in synaptic loss, impairing motor function recovery in SCI mice. Through high-content screening, we identified bazedoxifene as a potential therapeutic candidate that significantly attenuates lipid droplet accumulation within foam cells. This reduction in lipid load diminishes C1q expression by foam cells, thereby mitigating synaptic pathology and promoting synaptic preservation near the injury site. Our findings establish a novel connection between lipid metabolism and C1q-dependent synaptic damage, providing new insights into the mechanisms by which macrophages hinder functional recovery after SCI.
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