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Sleep-wake cycle, aging and cancer
Farhad F. Shadan
Jazyk angličtina Země Česko
Typ dokumentu přehledy
NLK
Free Medical Journals
od 2003 do 2013
Freely Accessible Science Journals
od 2003 do 2013
ROAD: Directory of Open Access Scholarly Resources
od 2002
- MeSH
- cirkadiánní rytmus fyziologie genetika imunologie MeSH
- diabetes mellitus 2. typu etiologie komplikace MeSH
- financování organizované MeSH
- hypertenze etiologie komplikace MeSH
- lidé MeSH
- medicína založená na důkazech trendy MeSH
- melatonin fyziologie metabolismus MeSH
- nádory etiologie komplikace MeSH
- obezita etiologie komplikace MeSH
- poruchy cirkadiánního rytmu (spánek) patofyziologie patologie MeSH
- stárnutí fyziologie imunologie patologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- přehledy MeSH
Disruptions in sleep-wake patterns have been linked to a variety of health problems, including an increase risk for obesity, type II diabetes, and hypertension. The link to increased risk of malignancy and premature aging is less clear, however. This manuscript reviews current epidemiological and experimental evidence linking alterations in sleep-wake patterns to malignancy and premature aging. Epidemiological evidence suggests that alterations in sleep-wake patterns (e.g.; night-shift or rotating-shift work) are associated with increases in leukemia, endometrial, breast, prostate, and colorectal cancers. Excessive long or short sleep duration is associated with increased mortality. These observations are further supported by experimental animal model systems: Sleep deprivation causes death in Drosophila cycle01 mutants. Manipulations of light-dark cycle in rodents or mutations that knock out certain genes in the circadian pathway accelerate aging and neoplastic growth. Melatonin, the pineal hormonal signal of darkness appears to have evolved in part to protect against mutagenesis by synchronizing cellular proliferation, differentiation, and apoptosis to the circadian peaks and troughs of genotoxic stress. A model based on circadian-gating of sleep-wake cycles, therefore, links the circadian pathway to the mutational theories of senescence and neoplasia.
Citace poskytuje Crossref.org
Lit.: 87
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- $a Disruptions in sleep-wake patterns have been linked to a variety of health problems, including an increase risk for obesity, type II diabetes, and hypertension. The link to increased risk of malignancy and premature aging is less clear, however. This manuscript reviews current epidemiological and experimental evidence linking alterations in sleep-wake patterns to malignancy and premature aging. Epidemiological evidence suggests that alterations in sleep-wake patterns (e.g.; night-shift or rotating-shift work) are associated with increases in leukemia, endometrial, breast, prostate, and colorectal cancers. Excessive long or short sleep duration is associated with increased mortality. These observations are further supported by experimental animal model systems: Sleep deprivation causes death in Drosophila cycle01 mutants. Manipulations of light-dark cycle in rodents or mutations that knock out certain genes in the circadian pathway accelerate aging and neoplastic growth. Melatonin, the pineal hormonal signal of darkness appears to have evolved in part to protect against mutagenesis by synchronizing cellular proliferation, differentiation, and apoptosis to the circadian peaks and troughs of genotoxic stress. A model based on circadian-gating of sleep-wake cycles, therefore, links the circadian pathway to the mutational theories of senescence and neoplasia.
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