Kisspeptin · research summary

Maternal Kisspeptin-10 Treatment Partially Rescues Fetal and Postnatal Cardiac Programming Disrupted by Maternal Hypothyroidism.

Cardiovascular toxicology · 2026. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

Experimental animal study using a rat model of maternal hypothyroidism
“MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.”

Subjects

Wistar rats (females and offspring)
“Adult Wistar rats (n = 48; 204 ± 14 g) from the Animal Breeding, Maintenance and Experimentation Laboratory (LaBIO) at the State University of Santa Cruz (UESC) were housed in plastic cages (6 animals/cage) under a 12 h light/12 h dark cycle at 22 ± 2 °C.”

Sample size

48 adult rats divided into three groups of 16 each
“Thus, three groups were formed: Control (n = 16), Hypothyroidism (n = 16) and Hypothyroidism + Kp10 (n = 16).”

Duration

From gestational day 0 to postnatal day 21
“Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.”

Reported findings

Maternal hypothyroidism reduced fetal and postnatal body and heart mass and impaired cardiomyocyte proliferation
“MH reduced fetal and postnatal body and heart mass, impaired cardiomyocyte proliferation, and dysregulated apoptotic and angiogenic markers.”
Maternal Kisspeptin-10 administration restored cardiomyocyte proliferation and nuclear density
“Maternal Kp10 administration enhanced postnatal weight gain, restored cardiomyocyte proliferation and nuclear density, and positively modulated apoptotic (Bax/Bcl2) and angiogenic (Vegf, Ang2, Flk1) pathways.”
Kisspeptin-10 administration increased redox and endoplasmic reticulum stress mediators in fetal hearts but reduced postnatal Chop expression
“However, it increased redox (8-OHdG) and endoplasmic reticulum (ER) stress (Grp78, Chop) mediators in fetal hearts, while reduced postnatal Chop expression in both sexes.”

Source: PubMed 42726152 · DOI 10.1007/s12012-026-10185-w · all study summaries

Reported findings

Maternal hypothyroidism reduced fetal and postnatal body and heart mass and impaired cardiomyocyte proliferation

“MH reduced fetal and postnatal body and heart mass, impaired cardiomyocyte proliferation, and dysregulated apoptotic and angiogenic markers.”

Maternal Kisspeptin-10 administration restored cardiomyocyte proliferation and nuclear density

“Maternal Kp10 administration enhanced postnatal weight gain, restored cardiomyocyte proliferation and nuclear density, and positively modulated apoptotic (Bax/Bcl2) and angiogenic (Vegf, Ang2, Flk1) pathways.”

Kisspeptin-10 administration increased redox and endoplasmic reticulum stress mediators in fetal hearts but reduced postnatal Chop expression

“However, it increased redox (8-OHdG) and endoplasmic reticulum (ER) stress (Grp78, Chop) mediators in fetal hearts, while reduced postnatal Chop expression in both sexes.”