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Whilst these observations suggest that TRF1 may be a suitable therapeutic target, they also raise questions regarding the function of TRF1 in telomere length maintenance and protection

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found that ferroptosis in ectopic endometrial stromal cells in patients with ovarian endometriosis could activate the p38 mitogen-activated protein kinase (p38 MAPK)/signal transducer and activator of transcription (STAT) 6 signalling pathway, thereby promoting local upregulation of vascular endothelial growth factor A (VEGFA) and interleukin-8 (IL-8) in ectopic lesions [15]

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