ReviewRedox biology2017
Proteostasis, oxidative stress and aging.
Review in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
136 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Effects of resveratrol on postmenopausal women: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Innovations in Skin and Soft Tissue Aging-A Systematic Literature Review and Market Analysis of Therapeutics and Associated Outcomes.Aesthetic plastic surgery · 2023Pooled it
- Association Between Composite Dietary Antioxidant Index and Asthma-Chronic Obstructive Pulmonary Disease Overlap Syndrome: Evidence From a Large Cohort in the UK Biobank.Food science & nutrition · 2026Article
- Effect of Gelatin-Peptide Complex from Sturgeon Skin on Behavioral, Antioxidant, and Neuroprotective Functions in D-Galactose-Induced Aging Mice: Thermal Degradation vs. Enzymatic Hydrolysis.Foods (Basel, Switzerland) · 2026Article
- Telomere Dysfunction and Proteostasis Decline Define Distinct Pathways of Cellular Senescence in the Human Respiratory Tract.Aging cell · 2026Article
- Valeric acid from oral microbiome suppresses esophageal cancer growth by disrupting eEF1A1 -mediated translational output.Nature communications · 2026Article
- Immune Aging as a Failure of Programmed Cell Death Coordination.International journal of molecular sciences · 2026Review
- Pathophysiology of reactive oxygen species (ROS).Archives of toxicology · 2026Review
- Antioxidant Nanozymes: From Rational Design to Biomedical Applications.Research (Washington, D.C.) · 2026Review
- Article
- Interplay of miR-243 and microbial interactions in aging and transgenerational immunity.Gut microbes · 2025Article
- Heme and iron toxicity in the aged spleen impairs T cell immunity through iron deprivation.Nature aging · 2025Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Association of the dietary inflammatory index with multi-organ biological age acceleration.Journal of health, population, and nutrition · 2025Article
- Silibinin Alleviates Liver Oxidative Stress in D-Galactose-Treated Kunming Mice via Microbiota Homeostasis in a Microbiota-Dependent Manner.Antioxidants (Basel, Switzerland) · 2025Article
- From Pathophysiology to Innovative Therapies in Eye Diseases: A Brief Overview.International journal of molecular sciences · 2025Review
- Article
- Major Oxidative and Antioxidant Mechanisms During Heat Stress-Induced Oxidative Stress in Chickens.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Proteome Reveals Metabolic Tuning by Restricted Insulin Signaling to Promote Longevity inBiology · 2025Article
- Age-associated microglial transcriptome leads to diminished immunogenicity and dysregulation of MCT4 and P2RY12/P2RY13 related functions.Cell death discovery · 2025Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed "proteostasis". Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the "ubiquitin-proteasomal system" (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the "autophagy-lysosomal system", which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells.
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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.