Kisspeptin-10

All ten cited papers are preclinical and were published in 2024 or 2025. The models vary widely: cerebral aneurysm formation, high-fat feeding in female mice, blood-brain barrier damage caused by the HIV Tat protein, gestational diabetes in rats, the blood-brain barrier after stroke, inflammatory senescence in cartilage cells, bone loss in knockout mice, reproduction in sterlet sturgeon and a forced swim test in male rats. The tenth is an analytical paper on detecting the peptide in urine, where it is of interest for doping control.

Several papers tied the reported effects to GPR54 or to a named pathway. In the aneurysm model, kisspeptin-10 acting through GPR54 lowered Egr-1 expression, and the authors reported less MMP-9, VEGF-A, macrophage infiltration and angiogenesis, with aneurysm development prevented. The bone study found osteoclast overactivity and bone loss in mice lacking Kiss1, Gpr54 or Dusp18, and reported that kisspeptin-10 suppressed osteoclast activity and bone loss in vivo. Blocking a pathway reversed the reported effects in four studies: a constitutively active RhoA mutant in the HIV Tat model, a cAMP inhibitor in the gestational diabetes model, SIRT1 silencing in the cartilage cells, and the kisspeptin antagonist peptide 234 in the rat forced swim test. In high-fat fed mice, beta-cell proliferation rose with no change in apoptosis; the stroke study linked barrier preservation to claudin-10 and Nrf2 signalling; and in sturgeon the peptide altered follicle maturation, gonadal steroids and plasma lipids. The detection study validated a liquid chromatography-mass spectrometry procedure for confirming the peptide in urine.

None of this work involves people, and most models appear only once in the list, so no finding here is replicated. Mechanisms were typically inferred by blocking one pathway within the same study that reported the effect. The sturgeon study concerns a fish species, and the entries shown give no group sizes or durations.