In skin tissue, PBM light is absorbed primarily by cytochrome c oxidase in keratinocytes and dermal fibroblasts, driving a cascade of photochemical events: increased electron transport chain efficiency leads to elevated ATP production and a controlled modulation of ROS. At therapeutic doses, this stimulates fibroblast activation and proliferation—the cells responsible for synthesizing the structural proteins of the dermis. Activated fibroblasts upregulate transcription of COL1A1 and COL3A1 genes, boosting type I and type III collagen production. Concurrently, PBM modulates matrix metalloproteinase (MMP) activity to reduce excess collagen degradation, and upregulates transforming growth factor-beta (TGF-β), a key driver of dermal remodeling. In the epidermis, PBM accelerates keratinocyte migration for wound re-epithelialization, reduces inflammatory cytokines (IL-1β, TNF-α), and may suppress melanogenesis pathways relevant to hyperpigmentation treatment.