Abstract

Age-related alteration of intracellular processes has been recognized as tipping of homeostatic balance towards increased entropy, reflected in, for instance, such hallmarks of aging as the loss of epigenetic information and disruption of proteostasis. Although the hallmarks of aging are useful for contextualizing geroscience research, the framework itself does not explain what fundamentally causes them to emerge in the first place. Herein, I propose a theorem that aims to explain the emergence of the hallmarks of aging as phenomena secondary to extracellular matrix chemical crosslinking, suggesting that the ensuant age-related extracellular matrix stiffening is a causative upstream agent in the aging process.