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10.18632/aging.103493

http://scihub22266oqcxt.onion/10.18632/aging.103493
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32534452!7346074!32534452
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suck abstract from ncbi

pmid32534452      Aging+(Albany+NY) 2020 ; 12 (11): 10004-10021
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  • From causes of aging to death from COVID-19 #MMPMID32534452
  • Blagosklonny MV
  • Aging (Albany NY) 2020[Jun]; 12 (11): 10004-10021 PMID32534452show ga
  • COVID-19 is not deadly early in life, but mortality increases exponentially with age, which is the strongest predictor of mortality. Mortality is higher in men than in women, because men age faster, and it is especially high in patients with age-related diseases, such as diabetes and hypertension, because these diseases are manifestations of aging and a measure of biological age. At its deepest level, aging (a program-like continuation of developmental growth) is driven by inappropriately high cellular functioning. The hyperfunction theory of quasi-programmed aging explains why COVID-19 vulnerability (lethality) is an age-dependent syndrome, linking it to other age-related diseases. It also explains inflammaging and immunosenescence, hyperinflammation, hyperthrombosis, and cytokine storms, all of which are associated with COVID-19 vulnerability. Anti-aging interventions, such as rapamycin, may slow aging and age-related diseases, potentially decreasing COVID-19 vulnerability.
  • |*Aging[MESH]
  • |Animals[MESH]
  • |Antifungal Agents/pharmacology/therapeutic use[MESH]
  • |COVID-19[MESH]
  • |Cellular Senescence[MESH]
  • |Coronavirus Infections/drug therapy/metabolism/*mortality[MESH]
  • |Cytokines/metabolism[MESH]
  • |Disease Susceptibility[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/drug therapy/metabolism/*mortality[MESH]


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