Adaptive Self-Defense of Mature Cells against Damage Is Based on the Warburg Effect, Dedifferentiation of Cells, and Resistance to Cell Death

This review analyzes the hypothesis of the preserved ability of various specialized mammalian cells to protect themselves from lethal injury by enacting a protective atavistic mechanism of cell dedifferentiation. The development of such a protection is accompanied by a transition of differentiated cells from the mitochondrial oxygen-dependent type of metabolism to reductive oxygen-independent metabolism (called the Warburg effect). This transition allows cells to increase the resistance to cell death from hypoxia, and can also induce the emergence of fetal markers characteristic of cell dedifferentiation. This paper, exemplified by the development of two pathologies (heart failure and type 2 diabetes), presents the findings that confirm the existence of such a mechanism and ways of its possible correction.