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Peer-reviewedCC BYFrontiers in endocrinology

Microglia as candidate links between hormonal signals and neuronal circuits in polycystic ovary syndrome: evidence gaps and a research agenda

  • Hongtao Li1
  • Tong Yin2
  • Yichen Wang1
  • Yixuan Wang3
  • Xiaoyuan Lin1
  • Xinyan Jia4
  • Wei Yi1
  • Han Yang1
4 affiliations
  1. 1South China Research Center for Acupuncture and Moxibustion, School of Acupuncture-Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine , , ,
  2. 2The Second Clinical Medical College, Guangzhou University of Chinese Medicine , , ,
  3. 3Tianjin University of Traditional Chinese Medicine , ,
  4. 4Shenzhen Bao'an Authentic TCM Therapy Hospital , , ,
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Abstract

Polycystic ovary syndrome (PCOS) combines reproductive endocrine dysfunction with metabolic, autonomic, and neurobehavioral phenotypes, yet the contribution of brain microglia remains uncertain. We conducted a structured narrative review that separates human PCOS evidence, PCOS-like animal findings, PCOS-related cellular observations, and non-PCOS mechanistic bridges. Only three heterogeneous PCOS-like studies directly assessed microglial outcomes, and none established a conserved microglial state, microglial necessity, a complete hormone–microglia–neuron causal chain, or human relevance. We therefore propose the PCOS Neuroimmune-Endocrine Triangular Network (PNETN), a falsifiable framework linking endocrine and metabolic signals, context-dependent microglial states, and neuronal circuits regulating GnRH/KNDy activity, luteinizing-hormone dynamics, ovulation, metabolism, autonomic function, and behavior. The framework defines criteria for causal promotion, including cell identity, regional specificity, temporal precedence, selective perturbation, rescue, orthogonal functional readouts, and independent replication. Microglia should currently be regarded as candidate contributors, not established clinical targets.

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Cite

BibTeXRIS
BibTeX
@article{li2026microglia,
  title = {{Microglia as candidate links between hormonal signals and neuronal circuits in polycystic ovary syndrome: evidence gaps and a research agenda}},
  author = {Hongtao Li and Tong Yin and Yichen Wang and Yixuan Wang and Xiaoyuan Lin and Xinyan Jia and Wei Yi and Han Yang},
  journal = {Frontiers in endocrinology},
  year = {2026},
  month = oct,
  doi = {10.3389/fendo.2026.1952469},
  url = {https://europepmc.org/article/PMC/PMC13673313},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Microglia as candidate links between hormonal signals and neuronal circuits in polycystic ovary syndrome: evidence gaps and a research agenda
AU  - Hongtao Li
AU  - Tong Yin
AU  - Yichen Wang
AU  - Yixuan Wang
AU  - Xiaoyuan Lin
AU  - Xinyan Jia
AU  - Wei Yi
AU  - Han Yang
PY  - 2026
DA  - 2026/10/02
JO  - Frontiers in endocrinology
DO  - 10.3389/fendo.2026.1952469
UR  - https://europepmc.org/article/PMC/PMC13673313
AB  - Polycystic ovary syndrome (PCOS) combines reproductive endocrine dysfunction with metabolic, autonomic, and neurobehavioral phenotypes, yet the contribution of brain microglia remains uncertain. We conducted a structured narrative review that separates human PCOS evidence, PCOS-like animal findings, PCOS-related cellular observations, and non-PCOS mechanistic bridges. Only three heterogeneous PCOS-like studies directly assessed microglial outcomes, and none established a conserved microglial state, microglial necessity, a complete hormone–microglia–neuron causal chain, or human relevance. We therefore propose the PCOS Neuroimmune-Endocrine Triangular Network (PNETN), a falsifiable framework linking endocrine and metabolic signals, context-dependent microglial states, and neuronal circuits regulating GnRH/KNDy activity, luteinizing-hormone dynamics, ovulation, metabolism, autonomic function, and behavior. The framework defines criteria for causal promotion, including cell identity, regional specificity, temporal precedence, selective perturbation, rescue, orthogonal functional readouts, and independent replication. Microglia should currently be regarded as candidate contributors, not established clinical targets.
SN  - 1664-2392
ER  -