ReviewAntioxidants (Basel, Switzerland)2021
Mitochondrial Redox Metabolism: The Epicenter of Metabolism during Cancer Progression.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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
25 citing papers in PubMed, 33 citations in OpenAlex.
- Stable Isotope-Resolved Metabolomics in Elucidating Mitochondrial Metabolic Reprogramming and Therapeutic Targets.Biomedical chromatography : BMC · 2026Review
- Bioinformatic characterization of SLC25A39 across cancers with validation in hepatocellular carcinoma.Discover oncology · 2026Article
- Neonatal hyperoxia promotes macrophage senescence and lung injury via a p38MAPK-dependent secretome.American journal of respiratory cell and molecular biology · 2026Article
- Metabolic plasticity and optimal redox homeostasis are essential for efficient metastatic colonization.Molecular metabolism · 2026Article
- Inflammation and RONS Dysregulation by Redox Enzymes as Mechanistic Links in HIV-1-Cancer Comorbidity.Pathogens (Basel, Switzerland) · 2026Review
- Comparative transcriptome profiling of electrical and controlled atmosphere stunning in finishing pigs.Food science of animal resources · 2026Article
- Unveiling the inhibitory effects of tannic acid and doxorubicin combination on pyruvate kinase M2 in breast cancer cells.Frontiers in pharmacology · 2026Article
- Dairy-rich diet triggers hepatic α-synuclein pathology via the liver-brain axis in GBA1-related Parkinson's disease.NPJ Parkinson's disease · 2025Article
- GLRX2 polymorphism and oxidative stress levels impact urothelial bladder cancer outcomes.Scientific reports · 2025Article
- Prognostic Significance ofBiology · 2025Article
- Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial metabolic reprogramming in colorectal cancer: mechanisms of resistance and future clinical interventions.Cell death discovery · 2025Review
- Molecular Insights in the Anticancer Activity of Natural Tocotrienols: Targeting Mitochondrial Metabolism and Cellular Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2025Review
- Insights into Reproductive Immunology and Placental Pathology.International journal of molecular sciences · 2024Article
- Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective.International journal of molecular sciences · 2024Review
- Complex II ambiguities-FADHThe Journal of biological chemistry · 2024Review
- The Role of Sirtuin-1 (SIRT1) in the Physiology and Pathophysiology of the Human Placenta.International journal of molecular sciences · 2023Review
- Review
- Mitochondrial metabolism: a predictive biomarker of radiotherapy efficacy and toxicity.Journal of cancer research and clinical oncology · 2023Review
- IL-1RA promotes oral squamous cell carcinoma malignancy through mitochondrial metabolism-mediated EGFR/JNK/SOX2 pathway.Journal of translational medicine · 2023Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial redox metabolism is the central component in the cellular metabolic landscape, where anabolic and catabolic pathways are reprogrammed to maintain optimum redox homeostasis. During different stages of cancer, the mitochondrial redox status plays an active role in navigating cancer cells' progression and regulating metabolic adaptation according to the constraints of each stage. Mitochondrial reactive oxygen species (ROS) accumulation induces malignant transformation. Once vigorous cell proliferation renders the core of the solid tumor hypoxic, the mitochondrial electron transport chain mediates ROS signaling for bringing about cellular adaptation to hypoxia. Highly aggressive cells are selected in this process, which are capable of progressing through the enhanced oxidative stress encountered during different stages of metastasis for distant colonization. Mitochondrial oxidative metabolism is suppressed to lower ROS generation, and the overall cellular metabolism is reprogrammed to maintain the optimum NADPH level in the mitochondria required for redox homeostasis. After reaching the distant organ, the intrinsic metabolic limitations of that organ dictate the success of colonization and flexibility of the mitochondrial metabolism of cancer cells plays a pivotal role in their adaptation to the new environment.
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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.