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A comprehensive analysis of the mitochondrial metabolic processes that may facilitate ferroptosis, in addition to the mitochondrial defense systems (most notably GPX4) was recently conducted [127]

While EAE models have offered valuable insight into adaptive immune responses, demyelination, and axonal damage in MS, they fall short in replicating the full spectrum of human MS pathology, particularly the disease's onset and heterogeneity (Figure 5)

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KDM5A inhibited osteogenesis by repressing Runx2 expression via H3K4me3 [108], whereas KDM6A inhibited adipogenesis and promoted osteo/chondrogenesis of BM-MSCs [100]