Photobiomodulation (PBM), also known as low-level light therapy (LLLT), has been studied for nearly 50 years, but its mechanisms remain unclear. Recent research has identified several key mechanisms, including the role of cytochrome c oxidase (Cox) as a photoacceptor, which absorbs near-infrared light and increases electron transport, mitochondrial membrane potential, and ATP production. Other mechanisms involve light-sensitive ion channels, such as TRPV and TRP, which can be activated by light, leading to calcium influx and histamine release. PBM also activates signaling pathways involving reactive oxygen species (ROS), cyclic AMP (cAMP), and nitric oxide (NO), which can influence transcription factors like NF-κB and CREB, leading to gene expression changes related to cell proliferation, migration, and anti-inflammatory responses. PBM parameters, such as wavelength, irradiance, and dose, are critical for its effectiveness. Red and near-infrared light (600-1100 nm) is most effective due to its penetration through tissue. The biphasic dose response curve indicates that both low and high doses can be ineffective, with optimal effects at intermediate levels. PBM has been shown to stimulate proliferation in low doses and suppress in higher doses, highlighting the importance of dose control. PBM activates various effector molecules, including transforming growth factor (TGF-β), vascular endothelial growth factor (VEGF), and hepatocyte growth factor (HGF), which are involved in tissue repair and regeneration. It also modulates inflammatory responses by reducing pro-inflammatory cytokines and increasing anti-inflammatory mediators. Heat shock proteins (HSPs), such as HSP27 and HSP70, play a role in protecting cells from oxidative stress and modulating inflammation. PBM has been shown to influence cellular mechanisms, including inflammation, macrophage activation, and immune responses. It can suppress pro-inflammatory signals, such as PGE2 production, and promote anti-inflammatory effects. PBM also affects transcription factors like NF-κB and CREB, which regulate gene expression related to cell survival, proliferation, and tissue repair. Overall, PBM has broad applications in wound healing, pain relief, and tissue regeneration, with its effectiveness dependent on precise parameter control and understanding of its molecular mechanisms.Photobiomodulation (PBM), also known as low-level light therapy (LLLT), has been studied for nearly 50 years, but its mechanisms remain unclear. Recent research has identified several key mechanisms, including the role of cytochrome c oxidase (Cox) as a photoacceptor, which absorbs near-infrared light and increases electron transport, mitochondrial membrane potential, and ATP production. Other mechanisms involve light-sensitive ion channels, such as TRPV and TRP, which can be activated by light, leading to calcium influx and histamine release. PBM also activates signaling pathways involving reactive oxygen species (ROS), cyclic AMP (cAMP), and nitric oxide (NO), which can influence transcription factors like NF-κB and CREB, leading to gene expression changes related to cell proliferation, migration, and anti-inflammatory responses. PBM parameters, such as wavelength, irradiance, and dose, are critical for its effectiveness. Red and near-infrared light (600-1100 nm) is most effective due to its penetration through tissue. The biphasic dose response curve indicates that both low and high doses can be ineffective, with optimal effects at intermediate levels. PBM has been shown to stimulate proliferation in low doses and suppress in higher doses, highlighting the importance of dose control. PBM activates various effector molecules, including transforming growth factor (TGF-β), vascular endothelial growth factor (VEGF), and hepatocyte growth factor (HGF), which are involved in tissue repair and regeneration. It also modulates inflammatory responses by reducing pro-inflammatory cytokines and increasing anti-inflammatory mediators. Heat shock proteins (HSPs), such as HSP27 and HSP70, play a role in protecting cells from oxidative stress and modulating inflammation. PBM has been shown to influence cellular mechanisms, including inflammation, macrophage activation, and immune responses. It can suppress pro-inflammatory signals, such as PGE2 production, and promote anti-inflammatory effects. PBM also affects transcription factors like NF-κB and CREB, which regulate gene expression related to cell survival, proliferation, and tissue repair. Overall, PBM has broad applications in wound healing, pain relief, and tissue regeneration, with its effectiveness dependent on precise parameter control and understanding of its molecular mechanisms.