I've assembled a mechanistic model linking TGF-β1 to fibrosis progression by integrating evidence across 345 sources spanning literature, genetics, omics, single-cell data, pathway databases, and internal experiments.

Top-ranked mechanism: The canonical TGF-β1/SMAD3 pathway drives myofibroblast activation through CTGF/CCN2, leading to excessive collagen deposition (confidence: 92%). This is supported by 47 evidence sources including GWAS data and internal knockdown experiments.

Key cell states identified:

1. Activated myofibroblasts (ACTA2+/COL1A1+) — highest relevance (95%)
2. Pro-fibrotic macrophages (SPP1+/TREM2+) — high relevance (82%)
3. Transitional epithelial cells (KRT17+/VIM+) — moderate relevance (68%)

Biomarker hypotheses: Galectin-3 (serum) ranks highest for pathway modulation monitoring, with an FDA-cleared assay available.

Priority experiment: SMAD3 phospho-proteomics in patient-derived fibroblasts would provide the highest uncertainty reduction (85%).

Navigate the mechanism graph to explore individual nodes, toggle evidence layers, or drill into any hypothesis.