ArticleAging2012
Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin.
Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 2 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
162 citing papers in PubMed, 2 syntheses or guidelines pooled it, 279 citations in OpenAlex.
- Cosmetogenomics unveiled: a systematic review of AI, genomics, and the future of personalized skincare.Frontiers in artificial intelligence · 2025Pooled it
- Integrating Forensic Autopsies with Proteomic Profiling for Suicide Risk Assessment: A Comprehensive Review of Literature.Current neuropharmacology · 2025Pooled it
- Protein Post-Translational Modifications in UV-Induced Skin Damage.Experimental dermatology · 2026Review
- Ethnopharmacological and Antiaging Evaluation of Salvia cadmica: Modulation of MMP1/MMP3 and Collagen in Oxidative Stress-Induced Senescence.Chemistry & biodiversity · 2026Article
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- Alternative Polyadenylation Signatures Distinguish Maladaptive Right Ventricular Remodeling in Pulmonary Hypertension: Implications for RNA-Based Diagnostics and Therapeutics.British journal of biomedical science · 2026Article
- Danggui Buxue Decoction Attenuates HClinical, cosmetic and investigational dermatology · 2026Article
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Development and Functional Characterization of Recombinant Mussel Adhesive Protein for Anti-Oxidative and Anti-Aging Therapeutic Applications.International journal of molecular sciences · 2025Article
- Osteogenesis Imperfecta: A Look into the Cerebellum of the Brtl Murine Model.Molecular neurobiology · 2025Article
- Reduced Usage ofPhenomics (Cham, Switzerland) · 2025Article
- Exploiting dysregulated iron homeostasis to eradicate persistent high-grade serous ovarian cancer.Cell death discovery · 2025Article
- Avian Lifespan Network Reveals Shared Mechanisms and New Key Players in Animal Longevity.Aging cell · 2025Article
- A Comprehensive Multiomics Signature of Doxorubicin-Induced Cellular Senescence in the Postmenopausal Human Ovary.Aging cell · 2025Article
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- A lncRNA-mediated metabolic rewiring of cell senescence.Cell reports · 2025Article
- Effect of Maternal Probiotic and Piglet Dietary Tryptophan Level on Performance and Piglet Intestinal Health Parameters Pre-Weaning.Microorganisms · 2025Article
- KLRG1 identifies regulatory T cells with mitochondrial alterations that accumulate with aging.Nature aging · 2025Article
- Metabolism and metabolomics in senescence, aging, and age-related diseases: a multiscale perspective.Frontiers of medicine · 2025Review
102 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular senescence arrests the proliferation of mammalian cells at risk for neoplastic transformation, and is also associated with aging. However, the factors that cause cellular senescence during aging are unclear. Excessive reactive oxygen species (ROS) have been shown to cause cellular senescence in culture, and accumulated molecular damage due to mitochondrial ROS has long been thought to drive aging phenotypesin vivo. Here, we test the hypothesis that mitochondrial oxidative stress can promote cellular senescence in vivo and contribute to aging phenotypes in vivo, specifically in the skin. We show that the number of senescent cells, as well as impaired mitochondrial (complex II) activity increase in naturally aged mouse skin. Using a mouse model of genetic Sod2 deficiency, we show that failure to express this important mitochondrial anti-oxidant enzyme also impairs mitochondrial complex II activity, causes nuclear DNA damage, and induces cellular senescence but not apoptosis in the epidermis. Sod2 deficiency also reduced the number of cells and thickness of the epidermis, while increasing terminal differentiation. Our results support the idea that mitochondrial oxidative stress and cellular senescence contribute to aging skin phenotypes in vivo.
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What OpenQuestion holds
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.