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Clinically, Se deficiency correlates with mitochondrial dysfunction and pathological accumulation of ROS/mtROS in chondrocytes, which contributes to OA progression, as evidenced by significantly lower serum Se levels in OA patients compared to healthy controls [20]

Currently, there is an increasing focus on therapeutic strategies targeting the side branches of glycolysis, especially the serine/glycine (ser/gly) synthesis pathway, since it is upregulated in approximately 30% of all cancers, including GBM [21]

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Identification of novel lipid droplet factors that regulate lipophagy and cholesterol efflux in macrophage foam cells