ReviewFrontiers in cell and developmental biology2021
Regulation of Age-Related Protein Toxicity.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Proteasome dysfunction underlies HERC2-linked neurodevelopmental disorder with Angelman-like clinical features.Cell death discovery · 2026Article
- Expanding our understanding of synucleinopathies: proteinopathy, proteinopenia, and lipidopathy.The FEBS journal · 2025Review
- Convergence of orphan quality control pathways at a ubiquitin chain-elongating ligase.Molecular cell · 2025Article
- Small Heat Shock Proteins: Protein Aggregation Amelioration and Neuro- and Age-Protective Roles.International journal of molecular sciences · 2025Review
- Pathophysiological processes underlying hidden hearing loss revealed in Kcnt1/2 double knockout mice.Aging cell · 2024Article
- Tissue-specific landscape of protein aggregation and quality control in an aging vertebrate.Developmental cell · 2024Article
- Article
- Editorial: Mechanisms and Pathways Contributing to the Diversity of Aging Across the Tree of Life.Frontiers in cell and developmental biology · 2022Article
- ROS: Basic Concepts, Sources, Cellular Signaling, and its Implications in Aging Pathways.Oxidative medicine and cellular longevity · 2022Review
- Drosophila p38 MAPK interacts with BAG-3/starvin to regulate age-dependent protein homeostasis.Aging cell · 2021Article
- The Role of Protein S-Nitrosylation in Protein Misfolding-Associated Diseases.Life (Basel, Switzerland) · 2021Review
- Age-dependent shift in the de novo proteome accompanies pathogenesis in an Alzheimer's disease mouse model.Communications biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteome damage plays a major role in aging and age-related neurodegenerative diseases. Under healthy conditions, molecular quality control mechanisms prevent toxic protein misfolding and aggregation. These mechanisms include molecular chaperones for protein folding, spatial compartmentalization for sequestration, and degradation pathways for the removal of harmful proteins. These mechanisms decline with age, resulting in the accumulation of aggregation-prone proteins that are harmful to cells. In the past decades, a variety of fast- and slow-aging model organisms have been used to investigate the biological mechanisms that accelerate or prevent such protein toxicity. In this review, we describe the most important mechanisms that are required for maintaining a healthy proteome. We describe how these mechanisms decline during aging and lead to toxic protein misassembly, aggregation, and amyloid formation. In addition, we discuss how optimized protein homeostasis mechanisms in long-living animals contribute to prolonging their lifespan. This knowledge might help us to develop interventions in the protein homeostasis network that delay aging and age-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.