Luteolys

Luteolys is a term occasionally encountered to denote luteolysis—the regression of the corpus luteum in the ovary at the end of the luteal phase when pregnancy is not established. In modern physiology, the preferred term is luteolysis; luteolys is not widely used as standard nomenclature.

Luteolysis involves the decline of progesterone synthesis and structural breakdown of luteal tissue. In many mammals, a uterus-derived signal, prostaglandin F2 alpha (PGF2α), initiates luteolysis by promoting luteal cell death and suppressing luteotrophic support from the pituitary. The regression then proceeds from functional decline to cellular apoptosis and resorption of the corpus luteum. In humans and some primates, luteolysis is largely driven by withdrawal of luteinizing hormone (LH) support, with prostaglandins playing a contributory role rather than acting as the sole trigger.

Timing and outcomes: after ovulation, the corpus luteum remains active for about 12–14 days in the absence of fertilization, producing progesterone to maintain the endometrium; if fertilization does not occur, progesterone falls and menstruation begins. If pregnancy occurs, signaling from the embryo and placenta can rescue the corpus luteum to sustain early pregnancy until placental takeover.

Clinical relevance: knowledge of luteolysis underpins fertility management, timing of ovulation, and the use of prostaglandin analogs for veterinary reproduction and reproductive endocrinology. Research continues to refine understanding of species differences and the molecular pathways involved.