Liver Sinusoid Microenvironment (2D p5.js Engine)
Week 0 / 96
Hepatocytes
Lipid Droplets
ROS Free Radicals
Vitamin E Shield
Quiescent HSC
Active Myofibroblast
96-Week Clinical Timeline Scrubbing
Intervention Parameters & Real-Time Metrics
Daily Vitamin E Dosage (alpha-tocopherol)
300 IU/day
Low-dose clinical threshold: 300 IU/day. Quenches membrane ROS lipid peroxyl radicals upon contact.
Lipid Influx Rate (Caloric & Fatty Acid Load)
Moderate (2.5x)
Drives hepatocyte lipid droplet accumulation and steatosis progression.
Mitochondrial Oxidative Stress Load
High (3.0x)
Generates ROS particles, promoting TGF-beta signaling and stellate cell myofibroblast transition.
Liver Fat Fraction
38.0%
Steatosis: Moderate (S2)
ROS Oxidative Index
72 / 100
High Peroxidation Stress
Active HSC Myofibroblasts
18 cells
Active Collagen Secretion
Fibrosis Stage
Stage F2
Periportal Fibrosis
96-Week Biomarker Telemetry Curve
— Fat % — ROS — Fibrosis Index
Biochemical Reversal Mechanism
1
Peroxyl Radical Quenching
Low-dose daily Vitamin E (alpha-tocopherol, 300 IU/day) partitions into hepatocyte lipid droplets and plasma membranes, donating hydrogen atoms to quench lipid peroxyl radicals before membrane chain reaction damage occurs.
2
Hepatic Stellate Cell Deactivation
Reduction in cellular ROS halts TGF-beta1 inflammatory cascades. Hepatic stellate cells transition from proliferative, collagen-secreting myofibroblasts (magenta) back to quiescent, lipid-storing phenotypes (cyan).
3
Endogenous Matrix Remodeling
With active fibrogenesis suppressed over 96 weeks, tissue collagenases (MMPs) tip the turnover balance toward degradation, gradually dissolving extracellular collagen fiber meshes and reversing fibrosis stage (F2 → F1/F0).
96-Week Milestone Summary
✓ Reversal On Track| Milestone | Fat Fraction (%) | ROS Stress | Active HSC | Fibrosis Stage |
|---|
* Based on clinical trial outcomes over 96 weeks. Low-dose 300 IU/day demonstrates sustained reduction in liver triglyceride accumulation, ROS lipid peroxidation, and collagen density.