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Concomitantly, HIF-1 suppresses mitochondrial fatty acid oxidation by downregulating c-Myc and its targets, medium-chain and long-chain acyl-CoA dehydrogenases(MCAD/LCAD) and inhibiting the PTEN pathway (98, 99)

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)