Dermal white adipose tissue undergoes senescence-associated secretory phenotype (SASP) changes that actively degrade extracellular matrix proteins and disrupt fibroblast function, rather than simply shrinking with age. These aging fat cells create an adipocyte-immune-fibroblast signaling network that amplifies tissue-level aging through chronic inflammation and altered adipokine secretion patterns. This mechanistic insight fundamentally challenges the traditional view of skin aging as primarily an epidermal and dermal phenomenon. The finding explains why volume-replacement therapies often fail—they address symptoms rather than the underlying adipocyte dysfunction driving the aging cascade. Regional differences in dermal fat explain why facial aging occurs unevenly across anatomical sites. The research opens therapeutic pathways through senolytics that clear senescent fat cells, senomorphics that suppress their inflammatory output, or metabolic reprogramming approaches. This represents a paradigm shift from treating skin aging superficially to targeting its metabolic roots. However, the framework remains largely theoretical, requiring clinical validation of adipocyte-targeted interventions and demonstration that manipulating fat cell function can meaningfully reverse skin aging in humans rather than just laboratory models.