ReviewRedox biology2013
Upregulation of the mitochondrial Lon Protease allows adaptation to acute oxidative stress but dysregulation is associated with chronic stress, disease, and aging.
Review in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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.
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Who cites it
77 citing papers in PubMed, 139 citations in OpenAlex.
- Mechanisms of Biological Aging with Special Reference to the Skeletal Muscle.Advances in experimental medicine and biology · 2025Review
- The Interplay between von Hippel-Lindau Tumor Suppressor Gene, Lon Protease, ROS Accumulation, and Inflammation in Clear Cell Renal Cell Carcinoma.Current issues in molecular biology · 2024Article
- Readdressing the Localization of Apolipoprotein E (APOE) in Mitochondria-Associated Endoplasmic Reticulum (ER) Membranes (MAMs): An Investigation of the Hepatic Protein-Protein Interactions of APOE with the Mitochondrial Proteins Lon Protease (LONP1), Mitochondrial Import Receptor Subunit TOM40 (TOMM40) and Voltage-Dependent Anion-Selective Channel 1 (VDAC1).International journal of molecular sciences · 2024Article
- Aging of alveolar type 2 cells induced byBiomolecules & biomedicine · 2024Article
- The effect of TLR3 priming conditions on MSC immunosuppressive properties.Stem cell research & therapy · 2023Article
- IPMK modulates FFA-induced insulin resistance in primary mouse hepatocytes.bioRxiv : the preprint server for biology · 2023Article
- Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet.International journal of molecular sciences · 2023Article
- Mitochondria as the Essence of Yang Qi in the Human Body.Phenomics (Cham, Switzerland) · 2022Review
- Posttranslational regulation of mitochondrial frataxin and identification of compounds that increase frataxin levels in Friedreich's ataxia.The Journal of biological chemistry · 2022Article
- Organismal and Cellular Stress Responses upon Disruption of Mitochondrial Lonp1 Protease.Cells · 2022Article
- The Mitochondrial Unfolded Protein Response: A Novel Protective Pathway Targeting Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial Lon protease is a gatekeeper for proteins newly imported into the matrix.Communications biology · 2021Article
- Mitochondrial ATP-Dependent Proteases-Biological Function and Potential Anti-Cancer Targets.Cancers · 2021Review
- The Age-Sensitive Efficacy of Calorie Restriction on Mitochondrial Biogenesis and mtDNA Damage in Rat Liver.International journal of molecular sciences · 2021Article
- Mitochondrial ROS promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mtDNA maintenance.Theranostics · 2021Article
- Changes in DNA methylation profiles of myalgic encephalomyelitis/chronic fatigue syndrome patients reflect systemic dysfunctions.Clinical epigenetics · 2020Article
- Selective knockdown of hexokinase 2 in rods leads to age-related photoreceptor degeneration and retinal metabolic remodeling.Cell death & disease · 2020Article
- Impact of Mitophagy and Mitochondrial Unfolded Protein Response as New Adaptive Mechanisms Underlying Old Pathologies: Sarcopenia and Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2020Review
- Intimate Relations-Mitochondria and Ageing.International journal of molecular sciences · 2020Review
- Redox Control of Proteolysis During Inactivity-Induced Skeletal Muscle Atrophy.Antioxidants & redox signaling · 2020Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The elimination of oxidatively modified proteins is a crucial process in maintaining cellular homeostasis, especially during stress. Mitochondria are protein-dense, high traffic compartments, whose polypeptides are constantly exposed to superoxide, hydrogen peroxide, and other reactive species, generated by 'electron leakage' from the respiratory chain. The level of oxidative stress to mitochondrial proteins is not constant, but instead varies greatly with numerous metabolic and environmental factors. Oxidized mitochondrial proteins must be removed rapidly (by proteolytic degradation) or they will aggregate, cross-link, and cause toxicity. The Lon Protease is a key enzyme in the degradation of oxidized proteins within the mitochondrial matrix. Under conditions of acute stress Lon is highly inducible, possibly with the oxidant acting as the signal inducer, thereby providing increased protection. It seems that under chronic stress conditions, however, Lon levels actually decline. Lon levels also decline with age and with senescence, and senescent cells even lose the ability to induce Lon during acute stress. We propose that the regulation of Lon is biphasic, in that it is up-regulated during transient stress and down-regulated during chronic stress and aging, and we suggest that the loss of Lon responsiveness may be a significant factor in aging, and in age-related diseases.
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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.