Figure 2.

A schematic of the interplay between mitochondria, telomere nucleo-protein complexes and proteo-biosynthesis regulation in response to cellular stress/damage. In response to the stress, the cell will decide how much fuel to burn and energy to expend to repair any damage accrued. If the cell can repair the damage it can progress through the cell cycle. Too much damage and the high risk of onconeogenesis induces cell death. Senescence, strictly in this simplified scenario, sees the cell carry accumulated, sub-lethal damage, as wear and tear, leaving the cell metabolically active, but physiologically non-contributory to the function of the tissue and organ in which it resides. The pervasive and overlapping roles that TERT (green) and magnesium (orange) play in targeting major components of the MRT trinity are highlighted. ER, mTOR/.