ArticleEMBO reports2020
N-acetyl-l-tyrosine is an intrinsic triggering factor of mitohormesis in stressed animals.
Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
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- Metabolic Adaptation during Cardiac Exercise Rehabilitation in Patients after a First Myocardial Infarction.Journal of proteome research · 2026Article
- Mammalian mitohormesis: from mitochondrial stressors to organismal benefits.The EMBO journal · 2025Review
- Stress-induced organismal death is genetically regulated by the mTOR-Zeste-Phae1 axis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unraveling the Relation of Parkinson's Disease and Metabolites: A Combined Analysis of Stool and Plasma Metabolites Based on Untargeted Metabolomics Technology.CNS neuroscience & therapeutics · 2025Article
- Exploring Therapeutic Targets for Age-Related Macular Degeneration From Circulating Proteins to Plasma Metabolites in the European Population.Translational vision science & technology · 2025Article
- Article
- N-Acetyltyrosine as a Biomarker of Parenteral Nutrition Administration in First-Tier Newborn Screening Assays.International journal of neonatal screening · 2024Article
- Redox regulation of UPR signalling and mitochondrial ER contact sites.Cellular and molecular life sciences : CMLS · 2024Review
- Drosophila cytokine GBP2 exerts immune responses and regulates GBP1 expression through GPCR receptor Mthl10.Insect biochemistry and molecular biology · 2024Article
- Developmental regulation of cellular metabolism is required for intestinal elongation and rotation.Development (Cambridge, England) · 2024Article
- The missing hallmark of health: psychosocial adaptation.Cell stress · 2024Article
- Causal relationship between human blood metabolites and risk of ischemic stroke: a Mendelian randomization study.Frontiers in genetics · 2024Article
- Exosomes from TNF-α preconditioned human umbilical cord mesenchymal stromal cells inhibit the autophagy of acinar cells of severe acute pancreatitis via shuttling bioactive metabolites.Cellular and molecular life sciences : CMLS · 2023Article
- Genome-microbiome interplay provides insight into the determinants of the human blood metabolome.Nature metabolism · 2022Article
- Using Metabolomics to Identify the Exposure and Functional Biomarkers of Ginger.Journal of agricultural and food chemistry · 2022Article
- The oxidative stress and metabolic response of Acinetobacter baumannii for aPDT multiple photosensitization.Scientific reports · 2022Article
- Glycolate combats massive oxidative stress by restoring redox potential in Caenorhabditis elegans.Communications biology · 2021Article
- N-acetyl-l-tyrosine is an intrinsic triggering factor of mitohormesis in stressed animals.EMBO reports · 2020Article
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6 authors at 2 institutions in 1 country.
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Abstract
Under stress conditions, mitochondria release low levels of reactive oxygen species (ROS), which triggers a cytoprotective response, called "mitohormesis". It still remains unclear how mitochondria respond to stress-derived stimuli and release a low level of ROS. Here, we show that N-acetyl-l-tyrosine (NAT) functions as a plausible intrinsic factor responsible for these tasks in stressed animals. NAT is present in the blood or hemolymph of healthy animals, and its concentrations increase in response to heat stress. Pretreatment with NAT significantly increases the stress tolerance of tested insects and mice. Analyses using Drosophila larvae and cultured cells demonstrate that the hormetic effects are triggered by transient NAT-induced perturbation of mitochondria, which causes a small increase in ROS production and leads to sequential retrograde responses: NAT-dependent FoxO activation increases in the gene expression of antioxidant enzymes and Keap1. Moreover, we find that NAT represses tumor growth, possibly via the activation of Keap1. In sum, we propose that NAT is a vital endogenous molecule that could serve as a triggering factor for mitohormesis.
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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.