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Factors such as mitochondrial dysfunction, ERS, and oxidative stress play critical regulatory roles in this process, while the neuro-glial cell interaction network further exacerbates neuronal damage

Animal studies show that selenium supplementation restores GPx activity in deficient models, reducing tissue damage from toxins

73,74 In addition, p53 induced ferroptosis required enzymatic activity of ALOX12, which is inhibited by SLC7A11, but independent of GPX4

While the IMM and matrix have long been the main focus of mitochondrial biology, the OMM is increasingly recognized as a critical platform for integrating cellular signals and coordinating communication between organelles [2]

This was carried out using a self-reported patient questionnaire to check for any possible contraindication to romosozumab therapy

Yet their paths diverge slightly when delving into specifics