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Overproduction of ROS is involved in the pathogenesis of acne vulgaris via various pathways, including activation of mTOR, peroxisome proliferator-activated receptors (PPARs), and toll-like receptors (TLRs) (21, 176178)

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Furthermore, the inhibition of ferroptosis represents a novel therapeutic target for OA management (152, 153)

Tumor endothelial cells have in some studies been observed to harbor similar somatic mutations as the malignant cells of the tumor, indicating a neoplastic origin [59, 73]

Fu Z, Xin X, Zhan Y, et al