Maternal Androgen Excess Inhibits Fetal Cardiomyocyte Proliferation Through RB-Mediated Cell Cycle Arrest and Induces Cardiac Hypertrophy in Adulthood

This study investigates the impact of maternal androgen excess on cardiac health in offspring, using pregnant mice injected with dihydrotestosterone (DHT). Results show that excessive androgen exposure in utero leads to thinner ventricular walls and decreased cardiomyocyte numbers in fetal offspring, causing cardiac hypertrophy and compromised cardiac function in adulthood. The study identifies that the androgen metabolite androsterone significantly increases in fetal heart tissue, leading to decreased phosphorylated retinoblastoma protein (pRB) and cell cycle-related proteins, resulting in cell cycle arrest and inhibited cardiomyocyte proliferation. The findings emphasize the importance of monitoring sex hormones during pregnancy and tracking cardiac function in offspring at risk of intrauterine androgen exposure.