ReviewBiogerontology2020
The crosstalk of NAD, ROS and autophagy in cellular health and ageing.
Review in Biogerontology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed, 46 citations in OpenAlex.
- Sirtuins in Medicine: Multifaceted Roles in Physiological Processes and Cardiovascular Diseases.Biomolecules · 2026Review
- NADInternational journal of molecular sciences · 2026Article
- Baicalein inhibits amyloid beta42 aggregation through disruption of the Asp23-Lys28 salt bridge.Scientific reports · 2025Article
- NADCells · 2025Review
- Interconnections of insulin/IGF-1 signaling and autophagy abnormalities in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- Natural Variation ofInternational journal of molecular sciences · 2025Article
- Bromodomain and extraterminal protein inhibitor JQ1 induces maturation arrest and disrupts the cytoplasmic organization in mouse oocytes under in vitro conditions.Scientific reports · 2025Article
- Simultaneous Live Mapping of pH and Hydrogen Peroxide Fluctuations in Autophagic Vesicles.JACS Au · 2025Article
- Autophagy-NADFrontiers in molecular biosciences · 2025Review
- Identification of Cellular Isoschaftoside-Mediated Anti-Senescence Mechanism inMolecules (Basel, Switzerland) · 2024Article
- SLC12A8 upregulation promotes colorectal cancer progression and chemoresistance.Translational cancer research · 2024Article
- Adverse Skeletal Muscle Adaptations in Individuals Born Preterm-A Comprehensive Review.Current issues in molecular biology · 2024Review
- Twelve-hour normothermic liver perfusion in a rat model: characterization of the changes in the ex-situ bio-molecular phenotype and metabolism.Scientific reports · 2024Article
- Resting natural killer cell homeostasis relies on tryptophan/NADEMBO reports · 2023Article
- Article
- Article
- Potential Synergistic Supplementation of NAD+ Promoting Compounds as a Strategy for Increasing Healthspan.Nutrients · 2023Review
- Premature senescence and cardiovascular disease following cancer treatments: mechanistic insights.Frontiers in cardiovascular medicine · 2023Review
- Autophagy promotes cell survival by maintaining NAD levels.Developmental cell · 2022Article
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 1 country.
Funding
Abstract
Cellular adaptation to various types of stress requires a complex network of steps that altogether lead to reconstitution of redox balance, degradation of damaged macromolecules and restoration of cellular metabolism. Advances in our understanding of the interplay between cellular signalling and signal translation paint a complex picture of multi-layered paths of regulation. In this review we explore the link between cellular adaptation to metabolic and oxidative stresses by activation of autophagy, a crucial cellular catabolic pathway. Metabolic stress can lead to changes in the redox state of nicotinamide adenine dinucleotide (NAD), a co-factor in a variety of enzymatic reactions and thus trigger autophagy that acts to sequester intracellular components for recycling to support cellular growth. Likewise, autophagy is activated by oxidative stress to selectively recycle damaged macromolecules and organelles and thus maintain cellular viability. Multiple proteins that help regulate or execute autophagy are targets of post-translational modifications (PTMs) that have an effect on their localization, binding affinity or enzymatic activity. These PTMs include acetylation, a reversible enzymatic modification of a protein's lysine residues, and oxidation, a set of reversible and irreversible modifications by free radicals. Here we highlight the latest findings and outstanding questions on the interplay of autophagy with metabolic stress, presenting as changes in NAD levels, and oxidative stress, with a focus on autophagy proteins that are regulated by both, oxidation and acetylation. We further explore the relevance of this multi-layered signalling to healthy human ageing and their potential role in human disease.
Indexed as
Identifiers
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.