luteolysis

Luteolysis is the regression of the corpus luteum (CL), the temporary endocrine gland formed after ovulation. The process ends progesterone production and leads to the decline of luteal tissue, allowing the cycle to progress to menstruation or to the next follicular phase.

The process comprises functional luteolysis, a rapid decline in progesterone synthesis by luteal cells, and structural luteolysis, the physical involution of the CL through cell death and vascular regression. Structural changes culminate in fibrous tissue replacement as the CL regresses.

In many nonprimate mammals, the uterus provides a luteolytic signal—prostaglandin F2 alpha (PGF2α)—which reaches the CL and triggers both functional and structural regression. The timing of luteolysis is coordinated with the end of the luteal phase and the absence of pregnancy. In pregnancy, signals from the conceptus (for example, interferon tau in ruminants) suppress uterine PGF2α production or action, thereby maintaining the CL.

In humans and some other primates, luteolysis is driven mainly by withdrawal of gonadotropic support (the fall in LH) and local luteolytic factors. Prostaglandin F2α may participate but is not the sole trigger. The corpus luteum typically regresses around day 11–14 of a luteal phase if pregnancy does not occur, with progesterone declining and menstruation following.

Clinical and agricultural relevance: luteolysis is central to the regulation of reproductive cycles and is exploited in livestock management using PGF2α analogs to synchronize estrus and treat luteal-related infertility. It also informs understanding of ovarian function and reproductive biology.