This paper explains that the kisspeptin receptor (Kiss1R) is a key protein that controls when puberty starts, how the body releases reproductive hormones, and how fertility works. Mutations that break this receptor can stop puberty and cause hormone problems. The system also links metabolism and the environment to reproductive health.

The kisspeptin receptor, Kiss1R, also known as Gpr54, is a G protein-coupled receptor (GPCR), deorphanized in 2001, when it was recognized as canonical receptor for the Kiss1-derived peptides, kisspeptins. In 2003, inactivating mutations of Kiss1R gene were first associated to lack of pubertal maturation and hypogonadotropic hypogonadism in humans and rodents. These seminal findings pointed out the previously unsuspected, essential role of Kiss1R and its ligands in control of reproductive maturation and function. This contention has been fully substantiated during the last decade by a wealth of clinical and experimental data, which has documented a fundamental function of the so-called Kiss1/Kiss1R system in the regulation of puberty onset, gonadotropin secretion and ovulation, as well as the metabolic and environmental modulation of fertility. In this review, we provide a succinct summary of some of the most salient facets of Kiss1R, as essential GPCR for the proper maturation and function of the reproductive axis.