Translophagy—A potential link between autophagy impairment and translational errors

Maintenance of protein homeostasis requires coordination between protein synthesis and degradation, yet whether autophagy directly controls translational machinery remains unclear. Here we explored whether autophagy maintains translational fidelity. Proteomic analysis of ubiquitin-enriched fractions and p62-associated proteins in autophagy-deficient tissue confirmed previous studies identifying ribosomal proteins and RNA-binding factors among candidate autophagy cargo. Pharmacological or genetic impairment of autophagy increased translational errors, particularly during oxidative stress. Components of the translational machinery localised to LC3-positive autophagic structures and accumulated in human brain tissue affected by neurodegeneration. These findings support a hypothesis in which autophagy preserves protein synthesis quality by removing damaged translational machinery. We term this proposed mechanism translophagy, potentially linking autophagy dysfunction, oxidative stress and the aberrant proteins in neurodegenerative disease.