ArticleMolecular biology of the cell2019
Cytosolic translational responses differ under conditions of severe short-term and long-term mitochondrial stress.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 72 citations in OpenAlex.
- Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026Review
- Perturbation of mitochondrial CaStress biology · 2026Article
- Mammalian mitohormesis: from mitochondrial stressors to organismal benefits.The EMBO journal · 2025Review
- Data-Independent Acquisition (DIA)-Based Label-Free Redox Proteomics (DIALRP) Identifies Prominent Cysteine Oxidations in Translation Machinery in Prostate Cancer Cells Under Oxidative Stress.Journal of proteome research · 2025Article
- Integrated analysis of transcriptional and metabolic responses to mitochondrial stress.Cell reports methods · 2025Article
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- Lysosome-Mitochondrial Crosstalk in Cellular Stress and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- UPRmt-regulated mitokines: novel strategies for myocardial injury repair.Frontiers in cell and developmental biology · 2025Review
- Detection of a Mitochondrial Fragmentation and Integrated Stress Response Using the Cell Painting Assay.Journal of medicinal chemistry · 2024Article
- Mitochondrial fusion and altered beta-oxidation drive muscle wasting in a Drosophila cachexia model.EMBO reports · 2024Article
- Prefoldin 2 contributes to mitochondrial morphology and function.BMC biology · 2023Article
- The unfolded protein response of the endoplasmic reticulum supports mitochondrial biogenesis by buffering nonimported proteins.Molecular biology of the cell · 2023Article
- Immunoproteasome-specific subunit PSMB9 induction is required to regulate cellular proteostasis upon mitochondrial dysfunction.Nature communications · 2023Article
- Mitoregulin Contributes to Creatine Shuttling and Cardiolipin Protection in Mice Muscle.International journal of molecular sciences · 2023Article
- PKR activation in mitochondrial unfolded protein response-mitochondrial dsRNA might do the trick.Frontiers in cell and developmental biology · 2023Article
- Review
- Inter-organellar and systemic responses to impaired mitochondrial matrix protein import in skeletal muscle.Communications biology · 2022Article
- Long-term mitochondrial stress induces early steps of Tau aggregation by increasing reactive oxygen species levels and affecting cellular proteostasis.Molecular biology of the cell · 2022Article
- Oxidative Stress-Induced Damage to the Developing Hippocampus Is Mediated by GSK3β.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Mitochondrial Inhibition by Sodium Azide Induces Assembly of eIF2α Phosphorylation-Independent Stress Granules in Mammalian Cells.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies demonstrated that cells inhibit protein synthesis as a compensatory mechanism for mitochondrial dysfunction. Protein synthesis can be attenuated by 1) the inhibition of mTOR kinase, which results in a decrease in the phosphorylation of S6K1 and 4E-BP1 proteins, and 2) an increase in the phosphorylation of eIF2α protein. The present study investigated both of these pathways under conditions of short-term acute and long-term mitochondrial stress. Short-term responses were triggered in mammalian cells by treatment with menadione, antimycin A, or CCCP. Long-term mitochondrial stress was induced by prolonged treatment with menadione or rotenone and expression of genetic alterations, such as knocking down the MIA40 oxidoreductase or knocking out NDUFA11 protein. Short-term menadione, antimycin A, or CCCP cell treatment led to the inhibition of protein synthesis, accompanied by a decrease in mTOR kinase activity, an increase in the phosphorylation of eIF2α (Ser51), and an increase in the level of ATF4 transcription factor. Conversely, long-term stress led to a decrease in eIF2α (Ser51) phosphorylation and ATF4 expression and to an increase in S6K1 (Thr389) phosphorylation. Thus, under long-term mitochondrial stress, cells trigger long-lasting adaptive responses for protection against excessive inhibition of protein synthesis.
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