ArticleCell cycle (Georgetown, Tex.)2013
MTOR-driven quasi-programmed aging as a disposable soma theory: blind watchmaker vs. intelligent designer.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Review
- Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- Neuronal mTORC1 inhibition promotes longevity without suppressing anabolic growth and reproduction in C. elegans.PLoS genetics · 2023Article
- The hyperfunction theory: An emerging paradigm for the biology of aging.Ageing research reviews · 2022Review
- Insights Into the Links Between Proteostasis and Aging FromFrontiers in aging · 2022Review
- Disordered Expression ofInternational journal of molecular sciences · 2019Article
- Gene expression and molecular pathway activation signatures ofOncotarget · 2017Article
- From rapalogs to anti-aging formula.Oncotarget · 2017Review
- Inverse correlation between longevity and developmental rate among wild C. elegans strains.Aging · 2016Article
- Epigenetic alterations in the suprachiasmatic nucleus and hippocampus contribute to age-related cognitive decline.Oncotarget · 2015Review
- Rejuvenating immunity: "anti-aging drug today" eight years later.Oncotarget · 2015Article
- Gerosuppression in confluent cells.Aging · 2014Article
- Signaling pathways activation profiles make better markers of cancer than expression of individual genes.Oncotarget · 2014Article
- Article
- Gerometabolites: the pseudohypoxic aging side of cancer oncometabolites.Cell cycle (Georgetown, Tex.) · 2014Article
- Quasi-programmed aging of budding yeast: a trade-off between programmed processes of cell proliferation, differentiation, stress response, survival and death defines yeast lifespan.Cell cycle (Georgetown, Tex.) · 2014Review
- Aging is not programmed: genetic pseudo-program is a shadow of developmental growth.Cell cycle (Georgetown, Tex.) · 2013Review
- Article
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Authors and funding
1 author.
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Abstract
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.
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