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Editorial
. 2021 Sep 17:8:103-107.
doi: 10.18632/oncoscience.545. eCollection 2021.

The hyperfunction theory of aging: three common misconceptions

Mikhail V Blagosklonny  1
Affiliations
Editorial

The hyperfunction theory of aging: three common misconceptions

Mikhail V Blagosklonny. Oncoscience. .
No abstract available

Keywords: cell senescence; geroconversion; geroscience; mTOR; quasi-program; rapamycin.

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Conflict of interest statement

CONFLICTS OF INTEREST Authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1. General presentation of hyperfunction theory.
Aging is a hyper-function caused by unnecessary and persistently activated signaling pathways, such as mTOR (for example), not by molecular damage. These signaling pathways activate cells, directly causing the development of age-related diseases. Aging is a sum of all diseases. Hyperfunctions may eventually lead to organ damage and loss of functions. Adopted with modifications from Figure 1 in ref. [1].
Figure 2
Figure 2. Absolute and relative hyperfunctions.
Optimal function is age-dependent.
Figure 3
Figure 3. Life-limiting aging.
(A) Normal Aging. Hyperfunctional (mTOR-driven) aging is life-limiting. It reaches a deadly threshold earlier than accumulating molecular damage does. (B) Premature aging syndromes. When artificially accelerated by gene knockouts, accumulation of molecular damage may become life-limiting. Adopted from ref. [10]).
Figure 4
Figure 4. Geroconversion model (in cell culture) displays basic features of hyperfunction theory.
(A) In proliferating cells, growth-promoting pathways such as mTOR drive cell mass growth, which is balanced by cell division. (B) When the cell cycle is suddenly blocked by p21 and p16, growth-promoting pathways such as mTOR drive geroconversion to senescence. Proliferation-like activity of mTOR in non-proliferating cells is a hyperfunction. Senescent cells display various hyperfunctions on a cellular level. See text for details.
See this image and copyright information in PMC

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References

    1. Blagosklonny MV. Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition. Cell Cycle. 2006; 5:2087–102. 10.4161/cc.5.18.3288. - DOI - PubMed
    1. Blagosklonny MV. TOR-driven aging: speeding car without brakes. Cell Cycle. 2009; 8:4055–59. 10.4161/cc.8.24.10310. - DOI - PubMed
    1. Blagosklonny MV. Rapamycin and quasi-programmed aging: four years later. Cell Cycle. 2010; 9:1859–62. 10.4161/cc.9.10.11872. - DOI - PubMed
    1. Blagosklonny MV. Answering the ultimate question “what is the proximal cause of aging?”. Aging (Albany NY). 2012; 4:861–77. 10.18632/aging.100525. - DOI - PMC - PubMed
    1. Gems D, de la Guardia Y. Alternative Perspectives on Aging in Caenorhabditis elegans: Reactive Oxygen Species or Hyperfunction? Antioxid Redox Signal. 2013; 19:321–29. 10.1089/ars.2012.4840. - DOI - PMC - PubMed

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