ArticleAging cell2020
Autophagic receptor p62 protects against glycation-derived toxicity and enhances viability.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- The interplay between vitamin D3 and Nrf2 signaling: mechanistic insights and therapeutic potentials.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Organic Germanium (Ge-132) Reduces Glycative Damage While Maintaining Cellular Stress Signaling, Revealing Limited Coordination Between Biochemical and Cellular Responses.Molecules (Basel, Switzerland) · 2026Article
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Predictable Modulation of a Spontaneous Post-translational Modification in Living Cells.Angewandte Chemie (International ed. in English) · 2025Article
- Retinal Autophagy for Sustaining Retinal Integrity as a Proof of Concept for Age-Related Macular Degeneration.International journal of molecular sciences · 2025Review
- Anti-Glycation and Anti-Aging Efficacy of Newly Synthesized Antioxidant With Autophagy Stimulating Activity.Journal of cosmetic dermatology · 2025Article
- Bufalin Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Macrophage Pyroptosis via P62 Pathway.Journal of cardiovascular translational research · 2025Article
- The chemical language of protein glycation.Nature chemical biology · 2025Review
- Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024Review
- Autophagy and UPS pathway contribute to nicotine-induced protection effect in Parkinson's disease.Experimental brain research · 2024Article
- An overview on glycation: molecular mechanisms, impact on proteins, pathogenesis, and inhibition.Biophysical reviews · 2024Review
- Article
- Proteopathy Linked to Exon-Skipping Isoform of RGR-Opsin Contributes to the Pathogenesis of Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2023Article
- Prolonged Exposure to High Glucose Induces Premature Senescence Through Oxidative Stress and Autophagy in Retinal Pigment Epithelial Cells.Archivum immunologiae et therapiae experimentalis · 2023Article
- Aquaporin 5 maintains lens transparency by regulating the lysosomal pathway using circRNA.Journal of cellular and molecular medicine · 2023Article
- Shu-Xie decoction alleviates oxidative stress and colon injury in acute sleep-deprived mice by suppressing p62/KEAP1/NRF2/HO1/NQO1 signaling.Frontiers in pharmacology · 2023Article
- Regulation of autophagy by natural polyphenols in the treatment of diabetic kidney disease: therapeutic potential and mechanism.Frontiers in endocrinology · 2023Review
- Proteostasis in aging-associated ocular disease.Molecular aspects of medicine · 2022Review
- Boosting proteolytic pathways as a treatment against glycation-derived damage in the brain?Neural regeneration research · 2022Article
- Selective Autophagy Receptor p62/SQSTM1, a Pivotal Player in Stress and Aging.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 3 countries.
Funding
Abstract
Diabetes and metabolic syndrome are associated with the typical American high glycemia diet and result in accumulation of high levels of advanced glycation end products (AGEs), particularly upon aging. AGEs form when sugars or their metabolites react with proteins. Associated with a myriad of age-related diseases, AGEs accumulate in many tissues and are cytotoxic. To date, efforts to limit glycation pharmacologically have failed in human trials. Thus, it is crucial to identify systems that remove AGEs, but such research is scanty. Here, we determined if and how AGEs might be cleared by autophagy. Our in vivo mouse and C. elegans models, in which we altered proteolysis or glycative burden, as well as experiments in five types of cells, revealed more than six criteria indicating that p62-dependent autophagy is a conserved pathway that plays a critical role in the removal of AGEs. Activation of autophagic removal of AGEs requires p62, and blocking this pathway results in accumulation of AGEs and compromised viability. Deficiency of p62 accelerates accumulation of AGEs in soluble and insoluble fractions. p62 itself is subject to glycative inactivation and accumulates as high mass species. Accumulation of p62 in retinal pigment epithelium is reversed by switching to a lower glycemia diet. Since diminution of glycative damage is associated with reduced risk for age-related diseases, including age-related macular degeneration, cardiovascular disease, diabetes, Alzheimer's, and Parkinson's, discovery of methods to limit AGEs or enhance p62-dependent autophagy offers novel potential therapeutic targets to treat AGEs-related pathologies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.