Preclinical (mouse model) · PMID 41955717
Kisspeptin-10 attenuates pulmonary arterial hypertension via restoration of mitochondrial function in pulmonary artery smooth muscle cells — VialBase Research
KP-10 attenuates PAH via GPR54 receptor in SU5416/hypoxia mouse model
Last updated · 2026 · Huang S, Chen Z, Gong W, Song Y, Ding W, Zhang L, Li J · Neuropeptides
Key findings
- KP-10 attenuates PAH via GPR54 receptor in SU5416/hypoxia mouse model
- Reduced right ventricular systolic pressure, hypertrophy, and vascular remodeling
- Restored mitochondrial membrane potential, ATP production, cytochrome c oxidase activity
- Normalized PINK1/Parkin/FUNDC1 mitophagy protein accumulation
- Inhibited hypoxia-induced PASMC proliferation in vitro
- Identifies Kisspeptin/GPR54 axis as potential PAH therapeutic target
PMID 41955717 — Kisspeptin-10 in Pulmonary Arterial Hypertension
Compound: Kisspeptin Citation: Huang S et al. Neuropeptides. 2026;117:102611. doi:10.1016/j.npep.2026.102611
Summary
Demonstrates that Kisspeptin-10, acting via GPR54, attenuates pulmonary arterial hypertension (PAH) in a mouse model by restoring mitochondrial function in pulmonary artery smooth muscle cells (PASMCs).
Key Findings
- In vivo: KP-10 reduced right ventricular systolic pressure, RV hypertrophy, and pulmonary vascular remodeling in SU5416/hypoxia PAH model
- Mitochondrial restoration: Restored membrane potential, ATP production, and cytochrome c oxidase activity in hypoxic PASMCs and PAH lungs
- Mitophagy normalization: Reduced excessive accumulation of PINK1, Parkin, and FUNDC1 proteins
- Anti-proliferative: Directly inhibited hypoxia-induced PASMC proliferation in vitro
Significance
Reveals a non-reproductive function of kisspeptin — mitochondrial protection in cardiovascular disease. The GPR54 axis represents a novel therapeutic target for PAH, expanding kisspeptin’s potential beyond reproductive endocrinology. Parallels with SS-31‘s mitochondrial mechanisms are notable.
See Also
- Parent compound: Kisspeptin
- Related compound: SS-31