ArticleScientific reports2018
Partial involvement of Nrf2 in skeletal muscle mitohormesis as an adaptive response to mitochondrial uncoupling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers, 1 of them a synthesis that pooled it.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- Chronic alcohol consumption exacerbates ischemia-associated skeletal muscle mitochondrial dysfunction in a murine model of peripheral artery disease.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Alternative oxidase causes cell type- and tissue-specific responses in mutator mice.Life science alliance · 2023Article
- Harmonizing Magnetic Mitohormetic Regenerative Strategies: Developmental Implications of a Calcium-Mitochondrial Axis Invoked by Magnetic Field Exposure.Bioengineering (Basel, Switzerland) · 2023Review
- Temporal dynamics of muscle mitochondrial uncoupling-induced integrated stress response and ferroptosis defense.Frontiers in endocrinology · 2023Article
- Effect of one-time high load exercise on skeletal muscle injury in rats of different genders: oxidative stress and mitochondrial responses.Acta cirurgica brasileira · 2022Article
- Ketone bodies: from enemy to friend and guardian angel.BMC medicine · 2021Review
- The KEAP1-NRF2 System in Healthy Aging and Longevity.Antioxidants (Basel, Switzerland) · 2021Review
- A Role of Stress Sensor Nrf2 in Stimulating Thermogenesis and Energy Expenditure.Biomedicines · 2021Review
- Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.Redox biology · 2021Review
- Management of Oxidative Stress: Crosstalk Between Brown/Beige Adipose Tissues and Skeletal Muscles.Frontiers in physiology · 2021Review
- Functional, proteomic and bioinformatic analyses of Nrf2- and Keap1- null skeletal muscle.The Journal of physiology · 2020Article
- Tris DBA ameliorates IgA nephropathy by blunting the activating signal of NLRP3 inflammasome through SIRT1- and SIRT3-mediated autophagy induction.Journal of cellular and molecular medicine · 2020Article
- Age-induced mitochondrial DNA point mutations are inadequate to alter metabolic homeostasis in response to nutrient challenge.Aging cell · 2020Article
- Health Effects of Coffee: Mechanism Unraveled?Nutrients · 2020Review
- Muscle-derived GDF15 drives diurnal anorexia and systemic metabolic remodeling during mitochondrial stress.EMBO reports · 2020Article
- Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology.Biomolecules · 2020Review
- Mitochondrial Dysfunction in Kidney Disease and Uremic Sarcopenia.Frontiers in physiology · 2020Review
- Crosstalk between Nrf2 signaling and mitochondrial function in Parkinson's disease.Molecular and cellular neurosciences · 2019Review
- Mitohormesis and metabolic health: The interplay between ROS, cAMP and sirtuins.Free radical biology & medicine · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is usually associated with various metabolic disorders and ageing. However, salutary effects in response to mild mitochondrial perturbations have been reported in multiple organisms, whereas molecular regulators of cell-autonomous stress responses remain elusive. We addressed this question by asking whether the nuclear factor erythroid-derived-like 2 (Nrf2), a transcription factor and master regulator of cellular redox status is involved in adaptive physiological responses including muscle mitohormesis. Using a transgenic mouse model with skeletal muscle-specific mitochondrial uncoupling and oxidative phosphorylation (OXPHOS) inefficiency (UCP1-transgenic, TG) we show that additional genetic ablation of Nrf2 abolishes an adaptive muscle NAD(P)H quinone dehydrogenase 1 (NQO1) and catalase induction. Deficiency of Nrf2 also leads to decreased mitochondrial respiratory performance although muscle functional integrity, fiber-type profile and mitochondrial biogenesis were not significantly altered. Importantly, Nrf2 ablation did not abolish the induction of key genes and proteins of muscle integrated stress response including the serine, one-carbon cycle, and glycine synthesis (SOG) pathway in TG mice while further increasing glutathione peroxidase (GPX) activity linked to increased GPX1 protein levels. Conclusively, our results tune down the functions controlled by Nrf2 in muscle mitohormesis and oxidative stress defense during mitochondrial OXPHOS inefficiency.
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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.