This review identifies three dynamic molecular processes — epigenetic drift, proteostasis collapse, and mitochondrial noise — as central drivers of cellular aging. We propose that these phenomena are not mere biomarkers but act as integrated conductors of biological time, progressively eroding information fidelity and temporal coordination within cellular systems. By integrating evidence from epigenomics, proteomics, and mitochondrial biology, we construct a unified framework in which aging emerges as multi-scale desynchronization of regulatory networks. This mechanistic perspective offers novel targets for interventions aimed at preserving or restoring systemic temporal coherence, moving beyond traditional damage-centric paradigms.