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Supporting this model, peripheral blood mononuclear cells from women with chronic pelvic pain release significantly greater amounts of IL-1 following lipopolysaccharide-induced TLR4 activation, compared with pain-free controls, indicating a state of peripheral immune hyper-responsiveness and systemic neuroimmune sensitization ( versus ectopic tissue implantation (Tsamantioti and Mahdy, 2025), both disorders exhibit abnormal endometrial progesterone signaling and chronic inflammatory signaling that may converge on a shared neuroimmune axis driving pelvic pain ( 4.5 Oxidative stress and pain sensitization There is growing evidence that oxidative stress may be involved in the multifactorial pathophysiology of PCOS, as it can synergize with heightened levels of basal proinflammatory signaling molecules to worsen the disease (Zeber-Lubecka et al., 2023)

Huang D, Wang Y, Thompson JW,Yin T, Alexander PB,Qin D,Mudgal P, Wu H,Liang Y

A review of global health data underscores the gravity of the situation: cardiovascular diseases have become the leading cause of global mortality, accounting for nearly 18 million deaths annually (Roth et al., 2020)

Additionally, the reduction in CoA levels and the GSH/GSSG ratio following erastin treatment in NINJ1-overexpressing cells were reversed by xCT restoration (Fig

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I., Sarti, P., Leandro, P