Metabolic syndrome is a real disease and premalignant state induced by oncogenic stresses to block malignant transformation.
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Summary
After a strong correlation established between the systemic DNA damage response to inhibit ongoing malignant transformation and metabolic syndrome characteristics, logical extrapolations for type 2 diabetes, cardiovascular disease, and aging are carried out.
- Type
- article
- Published
- 2010-06-01
- Cited by
- 8
- References
- 47
- OpenAlex
- https://openalex.org/W20097480
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:35352923
Keywords
Factor (programming language), Investment (military), Risk analysis (engineering), Business, Investment decisions
References
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- Are Paradoxical Cell Cycle Activities in Neurons and Glia Related to the Metabolic Theory of Alzheimer's Disease?
- Does a diagnosis of metabolic syndrome have value in clinical practice?
- Cellular senescence: when bad things happen to good cells
- Reactive Oxygen Species as Mediators of Cellular Senescence
- Inflammatory Signaling and Cellular Senescence
- Two faces of p53: aging and tumor suppression
- The power and the promise of oncogene-induced senescence markers
- Senescence, Wound Healing, and Cancer: the PAI-1 Connection
- Etoposide Induces ATM-Dependent Mitochondrial Biogenesis through AMPK Activation
- ROS and p53: a versatile partnership.
- Intrinsic tumour suppression
- Molecular signaling and genetic pathways of senescence: Its role in tumorigenesis and aging
- Mitogenic signalling and the p16INK4a–Rb pathway cooperate to enforce irreversible cellular senescence
- Induction of premature senescence in cardiomyocytes by doxorubicin as a novel mechanism of myocardial damage
- Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors.
- How does suppression of IGF-1 signaling by DNA damage affect aging and longevity?
- Antagonistic control of cell fates by JNK and p38-MAPK signaling
- Senescence comes of age
Cited by
- Deciphering the intricate regulatory mechanisms for the cellular choice between cell repair, apoptosis or senescence in response to damaging signals.
- Metabolic syndrome and neurotrophins: effects of metformin and non-steroidal antiinflammatory drug treatment.
- Insulin resistance: a potential marker and risk factor for active tuberculosis?
- Deregulation of the circadian clock constitutes a significant factor in tumorigenesis: a clockwork cancer. Part I: clocks and clocking machinery
- Genotoxic stress-mediated cell cycle activities for the decision of cellular fate
- p53 Mediates impaired insulin signaling in 3T3‐L1 adipocytes during hyperinsulinemia
- Impact of obesity and overweight on DNA stability: Few facts and many hypotheses.
- Metabolic Syndrome and Neurotrophins: Effects of Metformin and Non-Steroidal Antiinflammatory Drug Treatment Metabolik Sendrom ve Nörotrofinler: Metformin ve Non-Steroid Antienflamatuar İlaç Tedavisi Etkileri
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