Testosterone propionate protects against CCl4-induced liver fibrosis by maintaining mTOR-regulated autophagic flux via the LC3B/p62/Beclin-1 axis, preserving mitochondrial integrity; castration worsens fibrosis by impairing this pathway.
| Evidence tier | C Animal in vivo |
| Study type | 4 - Animal Study |
| Model system | Rat |
| Journal | Journal of Molecular Histology |
| Year | 2026 |
| Peer reviewed | Yes |
| Source | DOI 10.1007/s10735-026-10905-0 · PMID 42461311 |
In a CCl4-induced chronic liver injury rat model, testosterone propionate was found to preserve autophagic flux and mitochondrial function. Androgen deprivation worsened hepatic damage, while testosterone treatment maintained the LC3B/p62/Beclin-1/mTOR axis and protected mitochondrial quality control and reduced apoptosis.
| Intervention | Testosterone propionate |
| Target | mTOR / LC3B / p62 / Beclin-1 autophagy axis |
| Model | Rat |
| Effect | Testosterone maintains mTOR-regulated autophagy and mitochondrial integrity; androgen deprivation impairs autophagy and worsens liver fibrosis |