Testosterone propionate maintains autophagic flux and mitochondrial integrity via regulation of the LC3B/p62/Beclin-1/mTOR axis in induced liver fibrosis.
What this study shows
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.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Rat); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Rat |
| Journal | Journal of Molecular Histology |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1007/s10735-026-10905-0 · PMID 42461311 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| 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 |
In the Atlas
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- siRNA screening of the kinome identifies ULK1 as a multidomain modulator of autophagy (2007)
- ULK1 induces autophagy by phosphorylating Beclin-1 and activating VPS34 lipid kinase (2013)
- Reduced dietary protein intake does not alter autophagy in human blood: A randomized crossover study in healthy adults (2026)
- Role of Autophagy in Scleral Remodeling During Form-Deprivation Myopia (2026)
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