ArticleFree radical biology & medicine2010
Loss of manganese superoxide dismutase leads to abnormal growth and signal transduction in mouse embryonic fibroblasts.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 48 citations in OpenAlex.
- Mitochondrial antioxidant enzyme (SOD2) at the crossroads of redox signaling and cancer progression.Free radical research · 2026Review
- Silencing circRNA-ZFAND6 induces trophoblast apoptosis by activating the mitochondrial pathway through the miR-575/SOD2 axis in unexplained recurrent spontaneous abortion.BMC women's health · 2025Article
- The role of cytostatic in oxidative stress reactions.Frontiers in oncology · 2025Review
- Multiomics profiling reveals VDR as a central regulator of mesenchymal stem cell senescence with a known association with osteoporosis after high-fat diet exposure.International journal of oral science · 2024Article
- Alterations in Sod2-Induced Oxidative Stress Affect Endocrine Cancer Progression.The Journal of clinical endocrinology and metabolism · 2018Article
- Oxidative status of cardinal ligament in pelvic organ prolapse.Experimental and therapeutic medicine · 2018Article
- Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression.Cellular and molecular life sciences : CMLS · 2018Article
- Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling.The Journal of cell biology · 2018Review
- Manganese superoxide dismutase (SOD2): is there a center in the universe of mitochondrial redox signaling?Journal of bioenergetics and biomembranes · 2017Review
- Manganese Superoxide Dismutase Acetylation and Dysregulation, Due to Loss of SIRT3 Activity, Promote a Luminal B-Like Breast Carcinogenic-Permissive Phenotype.Antioxidants & redox signaling · 2016Review
- Telopodes of telocytes are influenced in vitro by redox conditions and ageing.Molecular and cellular biochemistry · 2015Article
- Mitochondrial hormesis and diabetic complications.Diabetes · 2015Review
- Regulation of MnSOD enzymatic activity by Sirt3 connects the mitochondrial acetylome signaling networks to aging and carcinogenesis.Antioxidants & redox signaling · 2014Review
- Oxidative stress-induced autophagy: role in pulmonary toxicity.Toxicology and applied pharmacology · 2014Review
- In vivo axonal transport deficits in a mouse model of fronto-temporal dementia.NeuroImage. Clinical · 2014Article
- CyclinB1/Cdk1 phosphorylates mitochondrial antioxidant MnSOD in cell adaptive response to radiation stress.Journal of molecular cell biology · 2013Article
- Association of copper-zinc superoxide dismutase (SOD1) and manganese superoxide dismutase (SOD2) genes with nonsyndromic myelomeningocele.Birth defects research. Part A, Clinical and molecular teratology · 2012Article
- Mouse Models of Oxidative Stress Indicate a Role for Modulating Healthy Aging.Journal of clinical & experimental pathology · 2012Article
- Polymorphic variations in manganese superoxide dismutase (MnSOD), glutathione peroxidase-1 (GPX1), and catalase (CAT) contribute to elevated plasma triglyceride levels in Chinese patients with type 2 diabetes or diabetic cardiovascular disease.Molecular and cellular biochemistry · 2012Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Manganese superoxide dismutase (MnSOD) in the mitochondria plays an important role in cellular defense against oxidative damage. Homozygous MnSOD knockout (Sod2(-/-)) mice are neonatal lethal, indicating the essential role of MnSOD in early development. To investigate the potential cellular abnormalities underlying the aborted development of Sod2(-/-) mice, we examined the growth of isolated mouse embryonic fibroblasts (MEFs) from Sod2(-/-) mice. We found that the proliferation of Sod2(-/-) MEFs was significantly decreased compared with wild-type MEFs despite the absence of morphological differences. The Sod2(-/-) MEFs produced less cellular ATP, had lower O(2) consumption, generated more superoxide, and expressed less Prdx3 protein. Furthermore, the loss of MnSOD dramatically altered several markers involved in cell proliferation and growth, including decreased growth stimulatory function of mTOR signaling and enhanced growth inhibitory function of GSK-3β signaling. Interestingly, the G-protein-coupled receptor-mediated intracellular Ca(2+) signal transduction was also severely suppressed in Sod2(-/-) MEFs. Finally, the ratio of microtubule-associated protein light chain 3 (LC3)-II/LC3-I, an index of autophagic activity, was increased in Sod2(-/-) MEFs, consistent with a reduction in mTOR signal transduction. These data demonstrate that MnSOD deficiency results in alterations in several key signaling pathways, which may contribute to the lethal phenotype of Sod2(-/-) mice.
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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.