Redox and Inflammatory Mechanisms in PMOS and Endometriosis: A Critical Review of Microbial and Plant-Derived Interventions
Review
OA: gold
public-domain-us
Abstract
BACKGROUND: Polycystic ovary syndrome (PCOS) or polyendocrine metabolic ovarian syndrome (PMOS) and endometriosis arise from different endocrine and tissue disturbances, yet oxidative stress (OS) and inflammation connect their initiating processes to reproductive dysfunction.
OBJECTIVE: In PMOS, redox-inflammatory signaling intersects with insulin resistance, androgen excess, and follicular dysfunction; in endometriosis, it supports estrogen-dependent lesion persistence, angiogenesis, and fibrosis. This narrative review examines these interactions and evaluates microbial and plant-derived interventions according to their mechanistic targets and clinical evidence.
KEY FINDINGS: Selected probiotic, synbiotic, and phytochemical trials in PMOS report improvements in metabolic, endocrine, and oxidative-inflammatory measures. In endometriosis, human intervention findings are concentrated in pain outcomes, while evidence for modulation of lesion biology remains predominantly experimental. Across both disorders, formulation, biological compartment, baseline phenotype, and concomitant treatment influence interpretation of therapeutic effects. Microbial metabolism offers a potential link between the two intervention classes by modifying phytochemical exposure and generating bioactive metabolites.
CONCLUSIONS: The evidence-informed comparative framework identifies where mechanistic findings have reached clinical evaluation and where further translation is needed. Future trials should connect standardized interventions and disease-specific clinical outcomes with measurements of microbial function and redox signaling to establish which patients benefit and through which pathways.
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Source provenance
- europepmc
- last seen: 2026-11-14T06:09:32.759907+00:00
- openalex
- last seen: 2026-11-14T06:02:37.066658+00:00
- pubmed
- last seen: 2026-11-14T06:04:18.320494+00:00
License: public-domain-us
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Courtesy of the U.S. National Library of Medicine
Courtesy of the U.S. National Library of Medicine