pathway
Cholesterol & Lipid Biology
ApoB particle burden, LDL retention, oxidized LDL, HDL function, triglycerides, macrophages, and plaque evolution.
Review layer
Last reviewed 2026-05-17
Systems teaching draft. Content is structured for education and graph expansion, with formal source tagging ready for the next review pass.
core
Systems Frame
This module presents lipids as structural, signaling, repair, immune, and vascular risk biology rather than a good-versus-bad cholesterol binary.
Core Concepts
Key Interactions
Insulin resistance raises triglyceride-rich lipoprotein pressure and alters lipid trafficking.
Oxidized LDL activates macrophages and can promote foam cell formation.
Inflammation and dyslipidemia reinforce vascular injury and endothelial activation.
HDL function is context-dependent and cannot be reduced to concentration alone.
Scenario Examples
sleep debt -> insulin resistance -> triglycerides
obesity -> macrophage activation -> dyslipidemia
ApoB retention -> endothelial injury