Reporter brief
Hepassocin prevents age-related liver senescence in mice via AMPK activation.
What happened
This preclinical study examined how Hepassocin (HPS), a hepatokine, affects liver aging and regeneration in mice. Aged HPS-knockout mice showed increased cellular senescence, impaired autophagy, and severely compromised liver regeneration after partial hepatectomy, with these deficits reversible by AMPK activation. The authors identified a signaling pathway (ANXA2-ERK-p90RSK-LKB1) through which HPS activates AMPK, and demonstrated that exogenous HPS improved regenerative outcomes in aged wild-type mice.
Why it matters
Assessment pending; this report does not establish a change in evidence.
What it does NOT prove
- Limitations have not been recorded; consult the primary source.
Study design and sample
Animal; Animal.
Aged mice (12 months old) and elderly humans; both HPS-knockout (KO) and wild-type littermates were studied
- Design
- Animal
- Sample
- —
- Journal
- Signal transduction and targeted therapy
- Published
- Sep 15, 2026
Effect size
Not recorded.
Caveats
- Assessment: Pending.
- Only the source material recorded on this evidence page was assessed.
Conflicts and funding
Not recorded.
Previous evidence
See the Rapamycin timeline and recorded assessment for prior evidence.
Primary source
Cancel Death charts and briefs may be reproduced editorially with attribution to CancelDeath.com. This brief is generated from the primary recorded source facts and assessment. Its review status is shown below; verify quotations against the paper before publication.