Year: 2026
Type: article
Abstract: 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.
Source: FEBS Letters
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $3,980
Funders: Procter and Gamble, Sumitomo Foundation, Uehara Memorial Foundation, Japan Agency for Medical Research and Development, Nippon Shinyaku, Alzheimer’s Research UK, Senri Life Science Foundation, Lotte Foundation, Medical Research Council, Biotechnology and Biological Sciences Research Council, Japan Society for the Promotion of Science
Awards: Interdisciplinary research on autophagy: From working principles to pathophysiology, AGEing and NuTrition Sensing (AGENT), Interrogating the autophagy-metabolism-cell death axis in iPSC-based Parkinson's disease models, 患者脳プロテオームに立脚した異染性白質ジストロフィーの病態分子機構解析, Targeting the autophagy-NAD axis in rare early-onset neurodegenerative diseases, G7484563823, G8409380342
OpenAlex ID: W7204484763
