An analysis of the mechanisms of phlegm-stasis and subthreshold lactate and lactate-modified levels in polycystic ovary syndrome, and research progress

Lactic acid, as a novel epigenetic regulator, participates in the regulation of gene transcription through lactylation. In the pathological context of PCOS, its core TCM pathogenesis—“the mutual entanglement of phlegm and blood stasis”—aligns closely with metabolic disorders and chronic low-grade inflammation in modern medicine. These conditions collectively drive the abnormal accumulation of lactate, which in turn acts as a substrate to drive lactylation, thereby continuously influencing the expression of genes related to ovarian granulosa cell function, follicular development, and endometrial receptivity. Abnormally accumulated lactate may not only represent the microscopic manifestation of “phlegm-dampness” but may also act as a signalling molecule that exacerbates the “blood stasis” state characterised by inflammation and tissue damage. Therefore, from the perspective of TCM's phlegm-blood stasis framework, it is essential to thoroughly investigate whether abnormalities in lactate metabolism and dysregulation of lactylation serve as common molecular nodes for key pathological processes in PCOS—such as insulin resistance (IR), chronic inflammation, and impaired follicular development. We also aim to explore the potential value of traditional Chinese medicine (TCM) and integrated Chinese-Western medicine strategies—guided by the therapeutic principle of “resolving phlegm and removing stasis”—in targeting the lactate metabolic network, with the goal of providing molecular-level evidence and new insights for the prevention and treatment of PCOS through integrated Chinese-Western medicine.