🍔 Hepatic Steatosis Progression Simulator

The Normal Hepatocyte

A healthy liver cell stores almost no visible fat.

• ~240 B: Hepatocytes per liver (the main liver cell type)
• <5%: Normal lipid content (of cell volume)
• ~1.5 kg: Liver mass (largest internal organ)
• High: Regeneration capacity (can regrow from partial loss)

A metabolic powerhouse

Hepatocytes process nutrients, toxins, and bile continuously.

Fat handling in balance

Fatty acid uptake and export normally stay balanced.

Why this cell matters

This single cell view anchors every later disease stage.

Lipid Droplets Begin to Accumulate

Excess energy intake pushes fat storage past a healthy limit.

• ~32%: Global MASLD prevalence (of adults worldwide)
• >5%: Steatosis threshold (hepatocyte fat by weight)
• High: Reversibility (with weight and diet change)
• Silent: Symptom burden (usually asymptomatic stage)

Droplets fill the cytoplasm

Triglycerides pack into growing round lipid droplets.

Driven by metabolic risk

Obesity, insulin resistance, and diet raise fat delivery.

Still a reversible stage

Simple steatosis alone rarely damages the cell yet.

Ballooning Degeneration and Inflammation

Overloaded hepatocytes swell, and immune cells rush in.

• ~5%: MASH prevalence (of adults worldwide)
• CK-18: Ballooning marker (cytoskeletal collapse signal)
• Kupffer: Key inflammatory cells (liver-resident macrophages)
• Elevated: Oxidative stress (lipotoxic cell injury)

The cell balloons

Cytoskeleton collapse makes the membrane swell and distort.

Immune cells infiltrate

Macrophages and lymphocytes cluster around injured hepatocytes.

A tipping point

MASH marks the shift from fat storage to injury.

Why it matters clinically

Only inflamed, ballooning livers tend to progress further.

Collagen Deposition Around the Cell

Repeated injury triggers scar-forming collagen around hepatocytes.

• F0–F4: Fibrosis staging (METAVIR scoring system)
• HSC: Key producer cell (activated hepatic stellate cells)
• Type I: Main collagen type (dominant scar protein)
• Duration: Progression driver (years of ongoing injury)

Stellate cells activate

Chronic injury turns quiet stellate cells into scar producers.

Fibers wrap the cell

Collagen strands encircle the hepatocyte in thin bands.

Time is the multiplier

Longer disease duration deposits denser collagen networks.

Dense Fibrotic Bands Replace Architecture

Scar tissue overwhelms the cell, replacing normal structure.

• F4: Fibrosis stage (cirrhosis, bridging scar bands)
• >1M/yr: Global cirrhosis deaths (end-stage liver disease)
• Low: Reversibility (architecture is largely fixed)
• HCC: Downstream risk (elevated liver cancer risk)

The cell is engulfed

Dense collagen bands surround and compress the hepatocyte.

Function is lost

Scar tissue replaces working liver architecture permanently.

The end stage

Cirrhosis is the final common pathway of chronic injury.