The effects of values-based digital microinterventions on mental health and valued living, and the role of photography and practice quality: A protocol for a randomized controlled trial.

The ovary serves as both the primary reproductive organ responsible for gamete production and a crucial endocrine gland in the female body. Its functions are essential for maintaining female fertility, the menstrual cycle, secondary sexual characteristics development, and systemic metabolic balance., However, the ovary does not operate in isolation; it interacts with multiple organs and systems, including adipose tissue, gut microbiota, and the pancreas, to collectively sustain female reproductive health and endocrine–metabolic homeostasis., Polycystic ovary syndrome (PCOS) is one of the most common endocrine and metabolic disorders in women of reproductive age, with a global prevalence of approximately 5%–20%. Recently, the condition has been proposed to be renamed “poly-metabolic ovarian syndrome (PMOS)”, shifting the paradigm from a singular gynecological endocrine disturbance to a multi-organ syndrome involving metabolic, cardiovascular, and neurological systems. The pathogenesis of PCOS is complex, with hyperandrogenemia, insulin resistance, and chronic inflammation constituting its core pathological features. These three factors interact in a cause-and-effect relationship, mutually reinforcing each other and forming a vicious cycle in the development of PCOS. Nevertheless, existing studies predominantly describe these pathways in isolation, focusing on associations between metabolic parameters and infertility risk, without mechanistically integrating the organ-level molecular crosstalk that underlies the PCOS pathological network. To date, it remains unclear how the “triad” of hyperandrogenemia, insulin resistance, and chronic inflammation mutually amplifies through positive feedback loops across organs and drives phenotypic heterogeneity. Based on the following criteria—(1) known anatomical or hormonal links with the ovary; (2) proven involvement in PCOS pathophysiology; and (3) participation in core regulation of the “triad”—this review systematically delineates the interactive mechanisms between the ovary and the hypothalamus (hypothalamic–pituitary–ovarian axis), adipose tissue, gut microbiota, pancreas, skeletal muscle, sympathetic nervous system, uterus, thyroid, adrenal glands, immune organs, and the circadian system. Focusing on the multi‑organ interactive network of the “triad”, we propose a conceptual framework of multi‑organ bidirectional positive‑feedback networks driven by the hyperandrogenemia–insulin resistance–chronic inflammation axis (). This integrative perspective aims to provide a mechanistic explanation for the phenotypic heterogeneity of PCOS and to offer a theoretical basis for developing precision therapeutic strategies that target organ‑crosstalk pathways.