Hirudin Anti-Pulmonary-Fibrosis (PGC1α / Sirt3)
Preclinical demonstration that hirudin attenuates idiopathic-pulmonary-fibrosis fibroblast senescence via the PGC1α / Sirt3 axis — He 2024 mouse model + primary lung fibroblasts.
Mechanistic Evidence Box
Preclinical / mechanistic- Page type
- Compound profile
- Evidence type
- Preclinical demonstration that hirudin attenuates idiopathic-pulmonary-fibrosis fibroblast senescence via the PGC1α / Sirt3 axis — He 2024 mouse model + primary lung fibroblasts.
- Evidence level
- Preclinical (animal)
- Drug vs leech
- Purified natural compound
- Safety domains
- Bleeding
Clinical translation limit
Hirudin's anti-pulmonary-fibrosis mechanism is established in mice and primary fibroblasts only. IPF is not an FDA-cleared K040187 indication; clinical translation requires randomised human trials with attention to bleeding risk.
Molecular Profile
- Category
- Other
- Evidence tier
- Preclinical
- Source species
- Hirudo medicinalis
- Discovered
- 2024 · He B et al.
Biological Targets
- → thrombin (primary); PGC1α / Sirt3 fibroblast-senescence pathway (downstream)
Key Citations
- He B et al. (2024), Biomedicines · PMID 39062010
External Resources
Related Other Compounds
Granulin (leech-derived)
Growth factor and wound-healing modulator — promotes angiogenesis and tissue regeneration.
Leech VEGF Modulator
Vascular endothelial growth factor pathway modulator — angiogenic and wound-healing implications.
Leech PDGF Modulator
Platelet-derived growth factor pathway modulator — implications for wound-healing.
Leech Granulin-A
Granulin-family peptide identified in Hirudo medicinalis — putative growth-factor / wound-healing analog (mechanistic only).