Lipid Lens
Foundations

Lipid Biology & Atherosclerosis

How the body moves fats around.

Meet the lipoproteins

Lipids don't dissolve in blood, so they travel as packages called lipoproteins. Each type has a different job.

Chylomicron~1000 nmApoB-48TG 92% · Chol 8%VLDL30–80 nmApoB-100TG 60% · Chol 40%IDL25–30 nmApoB-100TG 25% · Chol 75%LDL18–25 nmApoB-100TG 11% · Chol 89%HDL5–12 nmApoA-ITG 17% · Chol 83%TriglycerideCholesterol / cholesteryl esterPhospholipid monolayer
LDL
Low-density lipoprotein · “bad cholesterol”

LDL

Delivers cholesterol from the liver to peripheral tissues. When LDL particles are abundant or oxidized, they infiltrate the arterial wall and seed atherosclerotic plaque.

HDL
High-density lipoprotein · “good cholesterol”

HDL

Mediates reverse cholesterol transport — collecting excess cholesterol from tissues (including the artery wall) and returning it to the liver for disposal.

VLDL
Very-low-density lipoprotein

VLDL

Made by the liver, rich in triglycerides. As VLDL releases its triglyceride cargo to tissues, it shrinks and matures into IDL and then LDL.

Chylomicrons
Dietary fat transporters

Chylomicrons

Built in the intestine after a meal, chylomicrons ferry dietary triglycerides through the lymph and bloodstream to muscle and adipose tissue.

Lipoprotein lipase (LPL)

LPL is the enzyme — anchored to the inner surface of capillaries — that hydrolyzes triglycerides inside chylomicrons and VLDL, releasing free fatty acids for muscle to burn and for adipose tissue to store. Without functional LPL, triglycerides accumulate dramatically in plasma.

In plain language
Think of LPL as a pair of scissors that snips fat off circulating particles so your muscles and fat cells can use it.
Clinical detail
LPL deficiency (familial chylomicronemia syndrome) produces fasting triglycerides often > 1000 mg/dL which can increase pancreatitis risk. ApoC-II is a required cofactor; ApoC-III inhibits LPL — a target of newer triglyceride-lowering agents.

The atherosclerosis cascade

A six-step progression — from a healthy vessel to a ruptured plaque.

  1. 1

    Endothelial injury

    Hypertension, smoking, hyperglycemia, and elevated LDL particles damage the artery's smooth inner lining (the endothelium), making it more permeable.

  2. 2

    LDL infiltration & oxidation

    LDL particles slip through the damaged endothelium into the subendothelial space, where reactive oxygen species oxidize them — turning them into a potent inflammatory signal.

  3. 3

    Macrophage recruitment & foam cell formation

    Monocytes migrate into the wall and mature into macrophages. They engulf oxidized LDL via scavenger receptors and, unable to stop, fill with lipid droplets to become foam cells.

  4. 4

    Fatty streak

    Foam cells accumulate in the intima, forming the earliest visible lesion — a yellow fatty streak. These can appear even in adolescence.

  5. 5

    Fibrous plaque

    Smooth muscle cells migrate in and lay down collagen, building a fibrous cap over a growing lipid- and debris-rich necrotic core. The vessel begins to remodel and narrow.

  6. 6

    Rupture & thrombosis

    If the cap thins and tears, the highly thrombogenic core meets circulating platelets — triggering a clot that can occlude the artery and cause a heart attack or stroke.