From causes of aging to death from COVID-19

被引:85
|
作者
Blagosklonny, Mikhail V. [1 ]
机构
[1] Roswell Park Canc Inst, Buffalo, NY 14263 USA
来源
AGING-US | 2020年 / 12卷 / 11期
关键词
aging; mTOR; rapalogs; senolytics; SARS-CoV-2; COVID-19; coronavirus; MAMMALIAN TARGET; STEM-CELLS; CELLULAR SENESCENCE; RAPAMYCIN PATHWAY; CYTOKINE STORM; SKELETAL-MUSCLE; ANTIAGING DRUGS; AGE; INHIBITION; MTOR;
D O I
10.18632/aging.103493
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:10004 / 10021
页数:18
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