A redox-inflammasome threshold model of ovulation: a hypothesis on NLRP3-Mediated regulation

Ovulation is a highly coordinated biological process involving endocrine regulation, tissue remodeling, immune activation, metabolic adaptation, and redox signaling. Although inflammatory responses are recognized as essential components of follicular rupture, the mechanisms integrating oxidative stress, metabolic alterations, and inflammasome activation during ovulatory progression remain incompletely understood. Here, we propose a hypothesis-driven redox-inflammasome threshold model of ovulatory regulation, in which NLRP3 inflammasome signaling may serve as an important integrator of redox and metabolic cues that modulate inflammatory remodeling during the periovulatory period. This model suggests that successful ovulation requires a precisely balanced inflammatory threshold, whereas insufficient or excessive inflammasome activation may disrupt follicular homeostasis and contribute to ovarian dysfunction. Importantly, NLRP3 is proposed not as an indispensable determinant of follicular rupture, but as one regulatory component within a complex network involving cytokines, prostaglandins, matrix metalloproteinases, immune cells, and hormonal signals. By integrating current evidence linking mitochondrial reactive oxygen species, metabolic stress, and inflammation, this hypothesis provides a conceptual framework for understanding ovulation as a redox-sensitive immune-metabolic process. Future studies using cell type-specific NLRP3 manipulation, quantitative redox analysis, and single-cell approaches will be required to determine the physiological contribution of inflammasome signaling to ovulatory regulation.