ArticleCell death and differentiation2020
Chemical activation of SAT1 corrects diet-induced metabolic syndrome.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 38 citations in OpenAlex.
- Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2026Review
- Metabolic syndrome promotes endometrial cancer by Oleic acid-mediated polyamine accumulation.Nature communications · 2025Article
- Copper Homeostasis and Cuproptosis As Potential Intervention Strategy in Atherosclerosis.Journal of cardiovascular translational research · 2025Review
- Cuproptosis in prostate cancer: Molecular mechanisms, prognostic biomarkers and therapeutic frontiers of cuproptosis‑related genes (Review).International journal of oncology · 2025Review
- Cuproplasia and cuproptosis, two sides of the coin.Cancer communications (London, England) · 2025Review
- The central role of creatine and polyamines in fetal growth restriction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases.Apoptosis : an international journal on programmed cell death · 2024Review
- Targeting cuproplasia and cuproptosis in cancer.Nature reviews. Clinical oncology · 2024Review
- CheekAge, a next-generation epigenetic buccal clock, is predictive of mortality in human blood.Frontiers in aging · 2024Article
- Inhibition of Sat1 alleviates myocardial ischemia-reperfusion injury through regulation of ferroptosis via MAPK/ERK pathway.Frontiers in pharmacology · 2024Article
- Cuproptosis: mechanisms and links with cancers.Molecular cancer · 2023Review
- Review
- Phenylbutyrate modulates polyamine acetylase and ameliorates Snyder-Robinson syndrome in a Drosophila model and patient cells.JCI insight · 2022Article
- Autophagy in metabolism and quality control: opposing, complementary or interlinked functions?Autophagy · 2022Article
- Caloric restriction induced epigenetic effects on aging.Frontiers in cell and developmental biology · 2022Review
- Current Status of Autophagy Enhancers in Metabolic Disorders and Other Diseases.Frontiers in cell and developmental biology · 2022Review
- Probiotic induced synthesis of microbiota polyamine as a nutraceutical for metabolic syndrome and obesity-related type 2 diabetes.Frontiers in endocrinology · 2022Review
- New Insights into the Roles and Mechanisms of Spermidine in Aging and Age-Related Diseases.Aging and disease · 2021Review
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 8 institutions in 7 countries.
Funding
Abstract
The pharmacological targeting of polyamine metabolism is currently under the spotlight for its potential in the prevention and treatment of several age-associated disorders. Here, we report the finding that triethylenetetramine dihydrochloride (TETA), a copper-chelator agent that can be safely administered to patients for the long-term treatment of Wilson disease, exerts therapeutic benefits in animals challenged with hypercaloric dietary regimens. TETA reduced obesity induced by high-fat diet, excessive sucrose intake, or leptin deficiency, as it reduced glucose intolerance and hepatosteatosis, but induced autophagy. Mechanistically, these effects did not involve the depletion of copper from plasma or internal organs. Rather, the TETA effects relied on the activation of an energy-consuming polyamine catabolism, secondary to the stabilization of spermidine/spermine N
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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.