ArticleAging cell2018
Nrf2 stabilization prevents critical oxidative damage in Down syndrome cells.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 59 citations in OpenAlex.
- Effects of Resistance Training in Muscle Mass and Markers of Muscle Damage in Adults with Down Syndrome.International journal of environmental research and public health · 2021Trial
- Article
- Optimizing Brain Biology Through Near-Infrared-Induced Mitochondrial Melatonin Synthesis: A Hypothesis Paper.Cureus · 2026Review
- Nrf2 signaling pathway: focus on oxidative stress in osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025Review
- Oxidative Stress and Down Syndrome: A Systematic Review.Antioxidants (Basel, Switzerland) · 2025Review
- SARS-CoV-2 infection of human cortical cells is influenced by the interaction between aneuploidy and biological sex: insights from a Down syndrome in vitro model.Acta neuropathologica · 2025Article
- Oxidative stress biomarkers as novel screening tools for trisomy 21: a case-control study.BMC pregnancy and childbirth · 2025Article
- Review
- Nrf2 Signaling Pathway: Focus on Oxidative Stress in Spinal Cord Injury.Molecular neurobiology · 2025Review
- Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2.Biomolecules · 2025Review
- Mechanistic insights into Nrf2-driven pathogenesis and therapeutic targeting in spinal cord injury.Frontiers in immunology · 2025Review
- Oxidative Stress in Cataract Formation: Is There a Treatment Approach on the Horizon?Antioxidants (Basel, Switzerland) · 2024Review
- A dynamic in vitro model of Down syndrome neurogenesis with trisomy 21 gene dosage correction.Science advances · 2024Article
- The current insights of mitochondrial hormesis in the occurrence and treatment of bone and cartilage degeneration.Biological research · 2024Review
- Review
- The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023Review
- Assessing the effects of limestone dust and lead pollution on the ecophysiology of some selected urban tree species.Frontiers in plant science · 2023Article
- Oxidative-Stress-Associated Proteostasis Disturbances and Increased DNA Damage in the Hippocampal Granule Cells of the Ts65Dn Model of Down Syndrome.Antioxidants (Basel, Switzerland) · 2022Article
- DHPA Protects SH-SY5Y Cells from Oxidative Stress-Induced Apoptosis via Mitochondria Apoptosis and the Keap1/Nrf2/HO-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation.Journal of clinical medicine · 2022Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Mounting evidence implicates chronic oxidative stress as a critical driver of the aging process. Down syndrome (DS) is characterized by a complex phenotype, including early senescence. DS cells display increased levels of reactive oxygen species (ROS) and mitochondrial structural and metabolic dysfunction, which are counterbalanced by sustained Nrf2-mediated transcription of cellular antioxidant response elements (ARE). Here, we show that caspase 3/PKCδdependent activation of the Nrf2 pathway in DS and Dp16 (a mouse model of DS) cells is necessary to protect against chronic oxidative damage and to preserve cellular functionality. Mitochondria-targeted catalase (mCAT) significantly reduced oxidative stress, restored mitochondrial structure and function, normalized replicative and wound healing capacity, and rendered the Nrf2-mediated antioxidant response dispensable. These results highlight the critical role of Nrf2/ARE in the maintenance of DS cell homeostasis and validate mitochondrial-specific interventions as a key aspect of antioxidant and antiaging therapies.
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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.