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Peer-reviewedCC BY 4.0Journal of Lipid Research

Lipid signaling and foam cell formation in atherosclerosis and spinal cord injury

  • Guina Tan1,2,3
  • Xiaoxin Wang2,4
  • Jing Chen2,5
  • Ru Feng2,3,4
  • Hongyu Chu6
  • Degang Yang2,4
  • Jun Li2,4
  • Mingliang Yang2,4
  • Jianjun Li2,3,4,7
  • Ying Huang1
  • Feng Gao2,4
7 affiliations
  1. 1School of Rehabilitation, Gannan Medical University, Ganzhou City, Jiangxi Province, China
  2. 2Department of Spinal and Neural Functional Reconstruction, China Rehabilitation Research Center, Beijing, China
  3. 3Spinal Cord Injury Repair Laboratory, China Rehabilitation Science Institute, Beijing, China
  4. 4School of Rehabilitation, Capital Medical University, Beijing, China
  5. 5School of Rehabilitation, Wenzhou Medical University, Wenzhou City, Zhejiang Province, China
  6. 6Department of Rehabilitation Medicine, Peking University Hospital, Beijing, China
  7. 7Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
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Abstract

Macrophages and microglia serve as both “scavengers” and “immune sentinels” to maintain tissue homeostasis. However, when the lipid load exceeds their processing capacity, these cells transform into foam cells, thereby driving chronic inflammation and impairing tissue repair. Despite their distinct organ systems, atherosclerosis (AS) and spinal cord injury (SCI) converge on a common pathological cascade—foam cell formation—characterized by “enhanced lipid uptake, impaired cholesterol efflux, disrupted lysosomal/autophagic processing, and ER stress/reactive oxygen species/NLRP3-mediated inflammatory amplification.” This review systematically dissects and compares the molecular mechanisms underlying macrophage foaming in AS and SCI, with a particular focus on the similarities and differences in ABCA1/ABCG1-mediated cholesterol efflux, lipid droplet autophagy, the ER stress-NLRP3 axis, and nuclear receptor regulatory networks. Furthermore, it explores therapeutic avenues that target lipid metabolic reprogramming, including natural products, biomimetic nanomedicines, and genetic interventions. By establishing a cross-disease framework for lipid homeostasis disruption, this paper challenges traditional organ-centric views and provides a theoretical foundation that may accelerate the development of shared therapeutic strategies for AS and SCI.

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Cite

BibTeXRIS
BibTeX
@article{tan2026lipid,
  title = {{Lipid signaling and foam cell formation in atherosclerosis and spinal cord injury}},
  author = {Guina Tan and Xiaoxin Wang and Jing Chen and Ru Feng and Hongyu Chu and Degang Yang and Jun Li and Mingliang Yang and Jianjun Li and Ying Huang and Feng Gao},
  journal = {Journal of Lipid Research},
  year = {2026},
  month = sep,
  doi = {10.1016/j.jlr.2026.101153},
  url = {https://doi.org/10.1016/j.jlr.2026.101153},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Lipid signaling and foam cell formation in atherosclerosis and spinal cord injury
AU  - Guina Tan
AU  - Xiaoxin Wang
AU  - Jing Chen
AU  - Ru Feng
AU  - Hongyu Chu
AU  - Degang Yang
AU  - Jun Li
AU  - Mingliang Yang
AU  - Jianjun Li
AU  - Ying Huang
AU  - Feng Gao
PY  - 2026
DA  - 2026/09/21
JO  - Journal of Lipid Research
DO  - 10.1016/j.jlr.2026.101153
UR  - https://doi.org/10.1016/j.jlr.2026.101153
AB  - Macrophages and microglia serve as both “scavengers” and “immune sentinels” to maintain tissue homeostasis. However, when the lipid load exceeds their processing capacity, these cells transform into foam cells, thereby driving chronic inflammation and impairing tissue repair. Despite their distinct organ systems, atherosclerosis (AS) and spinal cord injury (SCI) converge on a common pathological cascade—foam cell formation—characterized by “enhanced lipid uptake, impaired cholesterol efflux, disrupted lysosomal/autophagic processing, and ER stress/reactive oxygen species/NLRP3-mediated inflammatory amplification.” This review systematically dissects and compares the molecular mechanisms underlying macrophage foaming in AS and SCI, with a particular focus on the similarities and differences in ABCA1/ABCG1-mediated cholesterol efflux, lipid droplet autophagy, the ER stress-NLRP3 axis, and nuclear receptor regulatory networks. Furthermore, it explores therapeutic avenues that target lipid metabolic reprogramming, including natural products, biomimetic nanomedicines, and genetic interventions. By establishing a cross-disease framework for lipid homeostasis disruption, this paper challenges traditional organ-centric views and provides a theoretical foundation that may accelerate the development of shared therapeutic strategies for AS and SCI.
SN  - 0022-2275
SN  - 1539-7262
ER  -