ReviewOpen biology2019
Protein damage, ageing and age-related diseases.
Review in Open biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 112 citations in OpenAlex.
- Antioxidative and chaperone-like activities of a bacterioruberin-rich extract: An innovative approach to protect the skin proteome.International journal of cosmetic science · 2026Article
- The brain and heart-axis in neurodegeneration and cardiovascular disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Oxidative Stress Footprints in Bone Marrow Mesenchymal Stem Cells from Untreated Advanced Breast Cancer.Oncology research · 2026Article
- Design principles of gene circuits for longevity.Trends in cell biology · 2025Review
- Decoding GNE Myopathy: From Molecular Basis to Therapeutic Advances.Annals of Indian Academy of Neurology · 2025Article
- Nuclear SUMOylation and Proteotoxic Stress Responses to Metals with Different Ligand Preferences.Chemical research in toxicology · 2025Article
- Assessment of membrane and metabolic parameters of erythrocytes exposed to selected bromophenols.Scientific reports · 2025Article
- Reduced UPF1 levels in senescence impair nonsense-mediated mRNA decay.Communications biology · 2025Article
- Empowering canonical biochemicals with cross-linked novelty: Recursions in applications of protein cross-links.Proteins · 2025Review
- Hidden route of protein damage through oxygen-confined photooxidation.Nature communications · 2024Article
- Nuclear pore and nucleocytoplasmic transport impairment in oxidative stress-induced neurodegeneration: relevance to molecular mechanisms in Pathogenesis of Parkinson's and other related neurodegenerative diseases.Molecular neurodegeneration · 2024Review
- Ageing-dependent thiol oxidation reveals early oxidation of proteins with core proteostasis functions.Life science alliance · 2024Article
- Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species.Heliyon · 2024Review
- Disrupted HSF1 regulation in normal and exceptional brain aging.Biogerontology · 2024Article
- Emerging insights into cuproptosis and copper metabolism: implications for age-related diseases and potential therapeutic strategies.Frontiers in aging neuroscience · 2024Review
- Neuronal Senescence in the Aged Brain.Aging and disease · 2023Review
- Morphometric and Nanomechanical Screening of Peripheral Blood Cells with Atomic Force Microscopy for Label-Free Assessment of Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Molecular Mechanisms of Resistance to Ionizing Radiation inAntioxidants (Basel, Switzerland) · 2023Article
- Age-related differences in response to plasma exchange in male rat liver tissues: insights from histopathological and machine-learning assisted spectrochemical analyses.Biogerontology · 2023Article
- Mutation and aging: news from the pool.Aging · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ageing is considered as a snowballing phenotype of the accumulation of damaged dysfunctional or toxic proteins and silent mutations (polymorphisms) that sensitize relevant proteins to oxidative damage as inborn predispositions to age-related diseases. Ageing is not a disease, but it causes (or shares common cause with) age-related diseases as suggested by similar slopes of age-related increase in the incidence of diseases and death. Studies of robust and more standard species revealed that dysfunctional oxidatively damaged proteins are the root cause of radiation-induced morbidity and mortality. Oxidized proteins accumulate with age and cause reversible ageing-like phenotypes with some irreversible consequences (e.g. mutations). Here, we observe in yeast that aggregation rate of damaged proteins follows the Gompertz law of mortality and review arguments for a causal relationship between oxidative protein damage, ageing and disease. Aerobes evolved proteomes remarkably resistant to oxidative damage, but imperfectly folded proteins become sensitive to oxidation. We show that α-synuclein mutations that predispose to early-onset Parkinson's disease bestow an increased intrinsic sensitivity of α-synuclein to in vitro oxidation. Considering how initially silent protein polymorphism becomes phenotypic while causing age-related diseases and how protein damage leads to genome alterations inspires a vision of predictive diagnostic, prognostic, prevention and treatment of degenerative diseases.
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What OpenQuestion holds
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.