ReviewRedox biology2021
Mitochondrial metabolism-mediated redox regulation in cancer progression.
Review in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
60 citing papers in PubMed, 98 citations in OpenAlex.
- Extracellular vesicle lipidomics liquid biopsy reveals systemic and tumor microenvironment metabolic reprogramming in ovarian cancer.Molecular oncology · 2026Article
- Quinoline-Based Scaffolds in Anticancer Drug Discovery: Molecular Targets, Synthetic Strategies, and Biological Advances.ChemMedChem · 2026Review
- Review
- SEMA4A promotes acute myeloid leukemia progression through inhibiting apoptosis.Genes & genomics · 2026Article
- Mitochondrial ribosomal protein MRPL27 supports glioma malignancy through regulation of oxidative phosphorylation.Cellular and molecular life sciences : CMLS · 2026Article
- Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription.BMC molecular and cell biology · 2026Article
- Nanomaterial-Mediated Targeting of Mitochondrial Metabolism: Strategies and Applications in Cancer Therapy.International journal of nanomedicine · 2026Review
- SLC25A39 identified as a key regulator of hepatocellular carcinoma progression through the mitochondrial ROS-cytochrome c-caspase signaling axis.Cellular & molecular biology letters · 2025Article
- Sirtuin 3 in diabetic kidney disease: mechanisms and pharmacotherapy.Renal failure · 2025Review
- Black phosphorus nanosheets boost mitochondrial oxidative phosphorylation improving immunotherapy outcomes.Nature nanotechnology · 2025Article
- GLRX2 polymorphism and oxidative stress levels impact urothelial bladder cancer outcomes.Scientific reports · 2025Article
- Oxidative phosphorylation and breast cancer progression: insights into PGC-1α's role in mitochondrial function.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Review
- The causal relationships between mitochondria and six types of cancer: a Mendelian randomization study.BMC cancer · 2025Article
- Acetylation suppresses breast cancer progression by sustaining CLYBL stability.Journal of translational medicine · 2025Article
- AsCurrent issues in molecular biology · 2025Article
- Photobiomodulation modulates mitochondrial energy metabolism and ameliorates neurological damage in an APP/PS1 mousmodel of Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Identification and validation of a prognostic signature of drug resistance and mitochondrial energy metabolism-related differentially expressed genes for breast cancer.Journal of translational medicine · 2025Article
- The roles of KRAS in cancer metabolism, tumor microenvironment and clinical therapy.Molecular cancer · 2025Review
- Smart Nanoarchitectures for Precision RNA Delivery: Harnessing Endogenous and Exogenous Stimuli in Cancer Treatment.Theranostics · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cells display abnormal metabolic activity as a result of activated oncogenes and loss of tumor suppressor genes. The Warburg Effect is a common metabolic feature of cancer that involves a preference for aerobic glycolysis over oxidative phosphorylation to generate ATP and building blocks for biosynthesis. However, emerging evidence indicates that mitochondrial metabolic pathways are also reprogrammed in cancer and play vital roles in bioenergetics, biosynthesis, and managing redox homeostasis. The mitochondria act a central hub for metabolic pathways that generate ATP and building blocks for lipid, nucleic acid and protein biosynthesis. However, mitochondrial respiration is also a leading source of reactive oxygen species that can damage cellular organelles and trigger cell death if levels become too high. In general, cancer cells are reported to have higher levels of reactive oxygen species than their non-cancerous cells of origin, and therefore must employ diverse metabolic strategies to prevent oxidative stress. However, mounting evidence indicates that the metabolic profiles between proliferative and disseminated cancer cells are not the same. In this review, we will examine mitochondrial metabolic pathways, such as glutaminolysis, that proliferative and disseminated cancer cells utilize to control their redox status.
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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.