ArticleTrends in biochemical sciences2016
SOD2 and the Mitochondrial UPR: Partners Regulating Cellular Phenotypic Transitions.
Article in Trends in biochemical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 45 citations in OpenAlex.
- Drug-induced metabolic remodeling promotes antimicrobial activity in macrophages and extends longevity in vivo.Life science alliance · 2026Article
- Comparative transcriptomic analysis of endometrial tissue associated with uterine fibroids and endometrial polyps.Scientific reports · 2026Article
- Discovery of tissue-specific proteomic signatures in juvenile dermatomyositis highlights pathways reflecting persistent disease activity, clinical heterogeneity, and myositis-specific autoantibody subtype.Annals of the rheumatic diseases · 2025Article
- Emerging roles of mitochondrial functions and epigenetic changes in the modulation of stem cell fate.Cellular and molecular life sciences : CMLS · 2024Review
- Mitochondrial inorganic polyphosphate is required to maintain proteostasis within the organelle.Frontiers in cell and developmental biology · 2024Article
- Effects of SIDT2 on the miR-25/NOX4/HuR axis and SIRT3 mRNA stability lead to ROS-mediated TNF-α expression in hydroquinone-treated leukemia cells.Cell biology and toxicology · 2023Article
- Overexpression of glutathione synthetase gene improving redox homeostasis and chicken infectious bursal disease virus propagation in chicken embryo fibroblast DF-1.Bioresources and bioprocessing · 2023Article
- Inhibitors of NLRP3 Inflammasome in Ischemic Heart Disease: Focus on Functional and Redox Aspects.Antioxidants (Basel, Switzerland) · 2023Review
- Enhancement of Tumor Cell Immunogenicity and Antitumor Properties Derived from Platinum-Conjugated Iron Nanoparticles.Cancers · 2023Article
- Insight into the mitochondrial unfolded protein response and cancer: opportunities and challenges.Cell & bioscience · 2022Review
- p53 regulates skeletal muscle mitophagy and mitochondrial quality control following denervation-induced muscle disuse.The Journal of biological chemistry · 2022Article
- Anakinra Activates Superoxide Dismutase 2 to Mitigate Inflammasome Activity.International journal of molecular sciences · 2021Article
- The Role and Mechanism of Oxidative Stress and Nuclear Receptors in the Development of NAFLD.Oxidative medicine and cellular longevity · 2021Review
- Can Metformin Exert as an Active Drug on Endothelial Dysfunction in Diabetic Subjects?Biomedicines · 2020Review
- Decoding the rosetta stone of mitonuclear communication.Pharmacological research · 2020Review
- Effect ofAntibiotics (Basel, Switzerland) · 2020Article
- A New Vision of Mitochondrial Unfolded Protein Response to the Sirtuin Family.Current neuropharmacology · 2020Review
- Mitohormesis, UPRCancer research · 2019Review
- New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis.Redox biology · 2019Review
- Mitochondrial function - gatekeeper of intestinal epithelial cell homeostasis.Nature reviews. Gastroenterology & hepatology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
ATP and reactive oxygen species (ROS) are signaling molecules that control cellular function and phenotype. Mitochondria produce both ATP and ROS. Since the electrons needed to generate either ATP or ROS originate from NADH/FADH2, the mechanism through which electrons flow towards oxygen determines yields and whether ATP or ROS prevails. Alterations in the electron flow impact cells dramatically, such as by supporting specialization (which requires high ATP) or imposing dedifferentiation. High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells. Here we propose that combined high mtH2O2 and mitochondrial unfolded protein response (UPR(mt)) activation are essential for somatic dedifferentiation programs and the acquisition of stem-like properties in reparative processes and disease.
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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.