ArticleAging cell2019
Improved mitochondrial stress response in long-lived Snell dwarf mice.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Oxidative Stress and Diminished Mitochondrial Proteostatic Reserve Are Linked to Enhanced mtUPR Initiation in Aged Mouse Muscle.Aging cell · 2026Article
- Synphilin-1 Is Essential for Cytoskeletal Integrity of Brain Ventricular Cilia and Mitochondrial Proteostasis.International journal of molecular sciences · 2026Article
- MICUs protect the heart by regulating mitochondrial calcium.Trends in pharmacological sciences · 2024Article
- Mitochondrial Quality Control via Mitochondrial Unfolded Protein Response (mtUPR) in Ageing and Neurodegenerative Diseases.Biomolecules · 2023Review
- Cardiovascular aging: the mitochondrial influence.The journal of cardiovascular aging · 2023Article
- Reducing mitochondrial ribosomal gene expression does not alter metabolic health or lifespan in mice.Scientific reports · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Effects of short-term endurance and strength exercise in the molecular regulation of skeletal muscle in hyperinsulinemic and hyperglycemic Slc2a4Cellular and molecular life sciences : CMLS · 2023Article
- mtUPR Modulation as a Therapeutic Target for Primary and Secondary Mitochondrial Diseases.International journal of molecular sciences · 2023Review
- Lamin A/C impairments cause mitochondrial dysfunction by attenuating PGC1α and the NAMPT-NAD+ pathway.Nucleic acids research · 2022Article
- Dietary regulation in health and disease.Signal transduction and targeted therapy · 2022Review
- Activation of the Mitochondrial Unfolded Protein Response: A New Therapeutic Target?Biomedicines · 2022Review
- Mitochondrial chaperones in human health and disease.Free radical biology & medicine · 2022Review
- From mutation to mechanism: deciphering the molecular function of genetic variants linked to human ageing.Briefings in functional genomics · 2022Article
- The Unfolded Protein Responses in Health, Aging, and Neurodegeneration: Recent Advances and Future Considerations.Frontiers in molecular neuroscience · 2022Review
- Drug triggered pruritus, rash, papules, and blisters - is AGEP a clash of an altered sphingolipid-metabolism and lysosomotropism of drugs accumulating in the skin?Lipids in health and disease · 2021Review
- Doxycycline promotes proteasome fitness in the central nervous system.Scientific reports · 2021Article
- Mitochondria and Antibiotics: For Good or for Evil?Biomolecules · 2021Review
- Flavin-Containing Monooxygenases Are Conserved Regulators of Stress Resistance and Metabolism.Frontiers in cell and developmental biology · 2021Article
- Challenging a "Cushy" Life: Potential Roles of Thermogenesis and Adipose Tissue Adaptations in Delayed Aging of Ames and Snell Dwarf Mice.Metabolites · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Prolonged lifespan and improved health in late adulthood can be achieved by partial inhibition of mitochondrial proteins in yeast, worms, fruit flies, and mice. Upregulation of the mitochondrial unfolded protein response (mtUPR) has been proposed as a common pathway in lifespan extension induced by mitochondrial defects. However, it is not known whether mtUPR is elevated in long-lived mouse models. Here, we report that Snell dwarf mice, which show 30%-40% lifespan extension and prolonged healthspan, exhibit augmented mitochondrial stress responses. Cultured cells from Snell mice show elevated levels of the mitochondrial chaperone HSP60 and mitochondrial protease LONP1, two components of the mtUPR. In response to mitochondrial stress, the increase in Tfam (mitochondrial transcription factor A), a regulator of mitochondrial transcription, is higher in Snell cells, while Pgc-1α, the main regulator of mitochondrial biogenesis, is upregulated only in Snell cells. Consistent with these differences, Snell cells maintain oxidative respiration rate, ATP content, and expression of mitochondrial-DNA-encoded genes after exposure to doxycycline stress. In vivo, compared to normal mice, Snell mice show stronger hepatic mtUPR induction and maintain mitochondrial protein stoichiometry after mitochondrial stress exposure. Overall, our work demonstrates that a long-lived mouse model exhibits improved mitochondrial stress response, and provides a rationale for future mouse lifespan studies involving compounds that induce mtUPR. Further research on mitochondrial homeostasis in long-lived mice may facilitate development of interventions that blunt mitochondrial deterioration in neurodegenerative diseases such as Alzheimer's and Parkinson's and postpone diseases of aging in humans.
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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.