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MTOR-driven quasi-programmed aging as a disposable soma theory

机译:MTOR驱动的准程序老化作为一次性体细胞理论

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摘要

If life were created by intelligent design, we would indeed age from accumulation of molecular damage. Repair is costly and limited by energetic resources, and we would allocate resources rationally. But, albeit elegant, this design is fictional. Instead, nature blindly selects for short-term benefits of robust developmental growth. “Quasi-programmed” by the blind watchmaker, aging is a wasteful and aimless continuation of developmental growth, driven by nutrient-sensing, growth-promoting signaling pathways such as MTOR (mechanistic target of rapamycin). A continuous post-developmental activity of such gerogenic pathways leads to hyperfunctions (aging), loss of homeostasis, age-related diseases, non-random organ damage and death. This model is consistent with a view that (1) soma is disposable, (2) aging and menopause are not programmed and (3) accumulation of random molecular damage is not a cause of aging as we know it.
机译:如果生命是通过智能设计创造的,那么我们确实会因分子损伤的积累而老化。维修成本高昂,并且受到精力充沛的资源的限制,我们将合理分配资源。但是,尽管优雅,但这种设计是虚构的。相反,自然盲目地选择了强劲的发展增长的短期利益。盲人钟表匠“准编程”的衰老是营养增长,促进生长的信号通路(例如MTOR(雷帕霉素的机械靶标))驱动的,浪费性的,漫无目的的持续发展。这种发源途径的持续的发育后活动导致机能亢进(衰老),体内稳态的丧失,与年龄有关的疾病,非随机器官损伤和死亡。该模型与以下观点相一致:(1)体是一次性的,(2)衰老和更年期没有编程,(3)随机分子损伤的积累不是我们所知的衰老原因。

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