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Increasing evidence indicates that these abnormalities are not independent phenomena but components of a self-perpetuating redox-endocrine network that sustains hyperandrogenism, anovulation, and metabolic impairment

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Usually, MyD88- and TRIF-dependent signaling pathways are triggered consecutively, due to the redistribution of the LPS-activated TLR4 from plasma membrane to the endosomes, leading to its lysosomal degradation and termination of the inflammatory response [24]

Was the evidence cellular, animal or human

10.1038/s41401-023-01151-1 70 LiF.MaoZ.DuY.CuiY.YangS.HuangK.et al (2024b)

This condition arises when the body lacks sufficient healthy red blood cells