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Abstract
Aging isn’t just wear and tear—it’s an ancient, layered program dating back hundreds of millions of years. In this article, we trace four distinct “aging systems” that emerged alongside key evolutionary leaps. First, early “plant-like” proto-animals relied on minimal ATP from fermentation and displayed simple structural breakdowns, still echoed in progeria’s fermentative shift. Then came mitochondria-driven life with explosive energy—and a second aging layer tied to oxidative damage in high-ATP tissues like brain and muscle. As multicellularity advanced, specialized DNA repair and apoptosis introduced a third aging choke point, seen in Cockayne syndrome and ataxia-telangiectasia. Finally, sexual reproduction and genes like WRN added the fourth “master” system, tying post-puberty decline to an organism’s broader fitness.
From the possibility that slow, rotary cilia gave rise to ATP synthase, to the genetic sabotage that reappears in progeroid diseases, these evolutionary tiers reveal why aging is so pervasive—and perhaps how we might intervene. Our framework explains why certain therapies target only parts of the puzzle and suggests that reprogramming factors (KLF4, Sox2, c-Myc, Oct4) tackle different layers of this ancient architecture. For evolutionary biologists, it reimagines aging as a deliberate, synergy-driven sequence; for gerontologists, it spotlights new angles for decelerating (or reversing) life’s final act.