ArticleGeroScience2021
High-intensity exercise training induces mitonuclear imbalance and activates the mitochondrial unfolded protein response in the skeletal muscle of aged mice.
Article in GeroScience, 2021. 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
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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.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Sprint interval exercise disrupts mitochondrial ultrastructure driving a unique mitochondrial stress response and remodelling in men.Nature communications · 2025Trial
- Exercise elicits mitonuclear protein imbalance and UPRJournal of physiology and biochemistry · 2026Article
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- Unfolding Resilience: Molecular Integration of the Integrated Stress Response and Mitochondrial UPR in Skeletal Muscle Homeostasis.Muscles (Basel, Switzerland) · 2026Review
- Exercise-induced modulation of the unfolded protein response: a therapeutic avenue for muscle wasting disorders.Journal of physiology and biochemistry · 2026Review
- Molecular Biomarkers of Training Responses: A Systems Framework for Exercise Adaptation and Athlete Monitoring.International journal of molecular sciences · 2026Review
- The role of exercise-mediated mitochondrial quality control remodeling in aging.Frontiers in cell and developmental biology · 2026Review
- ATF5-Dependent GDF15 Expression Mediates Anesthesia-Induced Neuroprotection Against Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Perturbation of multiprotein complexes in skeletal muscle induces protective proteases in the CNS that degrade pathogenic proteins.npj aging · 2025Article
- A Reassessment of Sarcopenia from a Redox Perspective as a Basis for Preventive and Therapeutic Interventions.International journal of molecular sciences · 2025Review
- Acute treadmill exercise induces mitochondrial unfolded protein response in skeletal muscle of male rats.Biochimica et biophysica acta. Bioenergetics · 2025Article
- Mitochondrial Unfolded Protein Response (mtUPR) and Diseases.Current medicinal chemistry · 2025Review
- Influence of upper-body high-intensity intermittent training on energy metabolism and maximal oxygen uptake in elite swimmers.Frontiers in physiology · 2025Article
- Mechanisms of the Mitochondrial Unfolded Protein Response in Caenorhabditis elegans and Mammals and Its Roles in Striated Muscles.Aging and disease · 2024Review
- Transgenic sensors reveal compartment-specific effects of aggregation-prone proteins on subcellular proteostasis during aging.Cell reports methods · 2024Article
- Research Progress on the Effect and Mechanism of Exercise Intervention on Sarcopenia Obesity.Clinical interventions in aging · 2024Review
- The multifaceted benefits of walking for healthy aging: from Blue Zones to molecular mechanisms.GeroScience · 2023Review
- Mitohormesis.Cell metabolism · 2023Review
- Impaired age-associated mitochondrial translation is mitigated by exercise and PGC-1α.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Intracellular to Interorgan Mitochondrial Communication in Striated Muscle in Health and Disease.Endocrine reviews · 2023Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impairment of mitochondrial metabolism is a hallmark of aging. Mitonuclear imbalance and the mitochondrial unfolded protein response (UPRmt) are two conserved mitochondrial mechanisms that play critical roles in ensuring mitochondrial proteostasis and function. Here, we combined bioinformatics, physiological, and molecular analyses to examine the role of mitonuclear imbalance and UPRmt in the skeletal muscle of aged rodents and humans. The analysis of transcripts from the skeletal muscle of aged humans (60-70 years old) revealed that individuals with higher levels of UPRmt-related genes displayed a consistent increase in several mitochondrial-related genes, including the OXPHOS-associated genes. Interestingly, high-intensity interval training (HIIT) was effective in stimulating the mitonuclear imbalance and UPRmt in the skeletal muscle of aged mice. Furthermore, these results were accompanied by higher levels of several mitochondrial markers and improvements in physiological parameters and physical performance. These data indicate that the maintenance or stimulation of the mitonuclear imbalance and UPRmt in the skeletal muscle could ensure mitochondrial proteostasis during aging, revealing new insights into targeting mitochondrial metabolism by using physical exercise.
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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.