## 1 Introduction
The diminished availability of ATP in nerve lesions triggers cell death and neurodegeneration since the low ATP level promotes neuronal depolarization, enhances neurotransmitter release, impairs ATP-dependent reuptake, and heightens the excitability of nociceptors [5; 6]. This phenomenon is further linked to the increased production of reactive oxygen species (ROS), which is exacerbated by the inflammation associated with neuronal damage. PBMT enhances the mitochondrial membrane potential (MMP), boosting electron transport. An elevated MMP typically increases ROS production, yet malfunctioning mitochondria also generate ROS via the \"ROS-induced ROS release\" (RIRR). Excessive oxidative stress triggers channels like the mitochondrial permeability transition pore and inner membrane anion channel, causing MMP to collapse and a heightened ROS via the electron transport chain [7]. This ROS surge may serve as a \"second messenger,\" activating RIRR in nearby mitochondria, compounding cellular harm. In NF-kB luciferase mice, a 810 nm laser PBM activated NF-kB, inducing ROS generation and a rise in ATP. N-acetylcysteine quenched ROS but not ATP, as PBM's MMP elevation increased ATP while provoking a ROS burst that likely activated NF-kB via protein kinase D [7]. PBM is thought to enhance mitochondrial function by increasing the mitochondrial membrane potential (MMP), leading to improved electron transport and adenosine triphosphate (ATP) production. Additionally, PBM can influence cellular signaling pathways, such as NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells), which play a central role in immune responses, inflammation, and cell survival. Transforming GrowthFactor Beta (TGF-\(\beta\)) is a multifunctional cytokine that regulates cell growth, differentiation, and immune responses. It is involved in various physiological processes, including tissue repair, wound healing, and immune modulation. TGF-\(\beta\) can stimulate fibroblast activity, leading to tissue remodeling and extracellular matrix production. In the context of PBM, TGF-\(\beta\) may play a role in mediating the effects of light therapy on tissue repair and regeneration, potentially enhancing the healing process and promoting favorable cellular responses [8]. The combination of PBM and TGF-\(\beta\) could have synergistic effects on tissue healing and regeneration. PBM may enhance the cellular responses to TGF-\(\beta\), leading to improved tissue repair and regeneration outcomes. However, the specific interactions between PBM and TGF-\(\beta\) in various therapeutic contexts would require further research to fully elucidate their combined effects and mechanisms of action [8]. The interaction between red and infrared light and photoacceptors such as cytochromes, water, lipids, S-nitrosylate, nitric oxide, and transient receptor potential channels (TRPC) that regulate that Ca\({}^{2+}\) passage, leads to a modification of the bioenergetic properties of mitochondria. This alteration includes adjustments in ATP and ROS generation, as well as the discharge of nitric oxide (NO) and calcium ions (Ca\({}^{2+}\)) at the mitochondrial level [5; 6]. The mechanism of action varies depending on the wavelength, which can either positively or negatively interfere with the photoacceptor resonances, influencing their conformation, properties, and activities. These findings strongly suggest that photobiomodulation plays a pivotal role in accelerating and enhancing the regeneration of damaged nerves [5; 6; 7; 8]. The article of [PERSON] et al. [9] explores the effects of photobiomodulation (PBM) on cellular pathways, including calcium regulation, through various interactions with chromophores. While mitochondrial chromophores and ROS signaling are key targets, alternative photoacceptors like water and TRP ion channels also play roles. The interconnectedness of calcium's roles in cell physiology aligns well with PBM's consistent effects across different life-forms.