Hepassocin prevents age-related liver senescence in mice via AMPK activation.
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.
What this changes
The finding has not established an approved change to our evidence assessment.
Source date: Sep 15, 2026 · Discovered: Sep 15, 2026 · Assessed: — · Research update
What it does not prove
- Limitations have not yet been verified. Read the primary source.
Extracted from supplied source material; model confidence is not a measured probability of correctness.
Study details
- Design
- Animal
- Sample size
- —
- Duration
- —
- Population
- Aged mice (12 months old) and elderly humans; both HPS-knockout (KO) and wild-type littermates were studied
- Primary outcome
- Liver regeneration capacity after partial hepatectomy (PHx) in aged mice, assessed by hepatocyte proliferation, liver mass recovery, and mortality
- Effect size
- —
- Significance
- Not reported
- Journal
- Signal transduction and targeted therapy
- Published
- Sep 15, 2026
Sources
Primary source
- Signal transduction and targeted therapy ↗Peer reviewed
Assessment history
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