Immune cytokines as a bridge linking the gut-liver-ovary axis in the pathogenesis of premature ovarian failure

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Premature ovarian failure (POF) is a multifactorial disorder characterized by the progressive decline of ovarian function, in which autoimmune factors account for approximately 10%-30% of cases. Accumulating evidence has demonstrated that immune-related mediators, including regulatory T cells (Tregs), interferon-γ (IFN-γ), and T helper 17 (Th17) cells, play pivotal regulatory roles in its initiation and progression. In recent years, the gut-liver axis and its potential mechanistic links with POF have emerged as a research hotspot in this field. Notably, these pathways are closely associated with the expression and functional balance of key immune mediators such as Tregs, IFN-γ, and Th17 cells. Based on the bridging role of immune cytokines between POF and the gut-liver axis, we propose a novel conceptual framework in which immune cytokines serve as a central hub to systematically elucidate the intrinsic connections among POF, gut microbiota dysbiosis, and bile acid metabolism. Furthermore, we highlight the current limitations of existing studies in this area. This perspective may provide a new theoretical framework for understanding the pathogenesis of POF and holds significant scientific value. Importantly, it may also offer novel insights and potential evidence for expanding clinical diagnostic and therapeutic strategies.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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