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From causes of aging to death from COVID-19

机译:从衰老的原因到COVID-19的死亡

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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.
机译:COVID-19并非生命早期的致命动物,但死亡率随年龄呈指数增长,这是死亡率的最强预测因子。男性的死亡率高于女性,这是因为男性的年龄更快,并且在患有与年龄有关的疾病(例如糖尿病和高血压)的患者中,死亡率尤其高,因为这些疾病是衰老的表现和生物学年龄的度量。在最深的层次上,衰老(程序性的生长发育持续性)是由细胞功能过高引起的。准程序性衰老的机能亢进理论解释了为什么COVID-19易感性(致死性)是一种年龄依赖性综合症,并将其与其他与年龄有关的疾病联系在一起的原因。它还解释了发炎和免疫衰老,过度发炎,血栓过多和细胞因子风暴,所有这些都与COVID-19脆弱性有关。雷帕霉素等抗衰老干预措施可能会延缓衰老和与年龄有关的疾病,从而可能降低COVID-19的脆弱性。

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