Near-to-perfect homeostasis: Examples of universal aging rule which germline evades


  • Nadiya M. Teplyuk

    Corresponding author
    1. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
    • Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM610, Boston, MA.
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Aging is considered to be a progressive decline in an organism's functioning over time and is almost universal throughout the living world. Currently, many different aging mechanisms have been reported at all levels of biological organization, with a variety of biochemical, metabolic, and genetic pathways involved. Some of these mechanisms are common across species, and others work different, but each of them is constitutive. This review describes the common characteristics of the aging processes, which are consistent changes over time that involve either the accumulation or depletion of particular system components. These accumulations and depletions may result from imperfect homeostasis, which is the incomplete compensation of a particular biological process with another process evolved to compensate it. In accordance with disposable-soma theory, this imperfection in homeostasis may originate as a function of cell differentiation as early as in yeasts. It may result either from antagonistic pleiotropy mechanisms, or be simply negligible as a subject of natural selection if an adverse effect of the accumulation phenotypically manifests in organism's post-reproductive age. If this phenomenon holds true for many different functions it would lead to the occurrence of a wide variety of aging mechanisms, some of which are common among species, while others unique, because aging is the inherent property of most biological processes that have not yet evolved to be perfectly in balance. Examples of imperfect homeostasis mechanisms of aging, the ways in which germ line escapes from them, and the possibilities of anti-aging treatment are discussed in this review. J. Cell. Biochem. 113: 388–396, 2012. © 2011 Wiley Periodicals, Inc.