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Mitochondrial membrane potential decreases after damage, making PTEN-induced Kinase1 (PINK1) accumulate and phosphorylate ubiquitin at Ser 65 in the outer mitochondrial membrane, which then recruits and binds Parkin proteins, thereby activating E3 ligase, resulting in more ubiquitination of outer mitochondrial membrane proteins, further driving the binding of ligands such as the autophagy adaptor protein Sequestosome 1 (PSQSTM1/P62), and finally making the autophagosome fuse with the damaged mitochondria to complete the mitochondrial autophagy process (Koyano et al., 2014)

Cellular Health: Traditionally associated with promoting optimal function of cells, fostering youthful resilience

Mitochondrial metabolism supports T cell anabolism by providing key metabolites for macromolecule synthesis and generating metabolites for T cell function