A liver protein declines with age and slows liver recovery in mice
Hepassocin (HPS), a protective protein made by the liver, decreases with aging in mice and elderly humans. When HPS was removed in aged mice, their livers showed more damage, slower recovery after injury, and impaired cellular cleanup; restoring HPS or activating its downstream pathway improved outcomes.
Why it matters: Age-related liver dysfunction increases disease risk and death, and identifying the molecular causes could lead to new treatments to restore liver health in older adults.
Keep in mind: This study was conducted in mice and elderly human samples; it is unclear whether boosting HPS would be safe or effective in treating human liver disease.
AI-assisted explanation based on the supplied abstract. Read the linked source for full context.
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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