Liver fibrosis is a significant global health issue characterized by the progressive accumulation of extracellular matrix (ECM), leading to hepatocyte dysfunction and disruption of liver architecture. This condition arises from hepatocyte injury and inflammatory cell infiltration, triggering the trans differentiation of hepatic stellate cells (HSCs) into myofibroblasts that produce collagen, contributing to fibrosis. A key factor in this pathology is the excessive production of reactive oxygen species (ROS) due to various insults such as toxic exposure or viral infection, which further exacerbate hepatocyte damage and fibrogenesis. The activation of nuclear factor-kappa B (NF-κB) amplifies the inflammatory response. Therapeutic interventions targeting oxidative stress and inflammation, such as the nuclear factor erythroid 2-related factor 2 (Nrf2) and peroxisome proliferator-activated receptor gamma (PPARγ) pathways, have shown promise in mitigating fibrosis by enhancing antioxidant defenses and regulating inflammatory processes. Additionally, photobiomodulation therapy (PBMT), particularly low-level laser therapy (LLLT), has emerged as a potential non-invasive approach to reduce oxidative stress and inflammation. However, the specific mechanisms by which LLLT affects liver fibrogenesis require further investigation. This review aims to explore the potential of Low-Level Laser Therapy (LLLT) in mitigating liver fibrosis by examining its impact on the activation of antioxidants and anti-inflammatory cytokines. It focuses on elucidating how LLLT may stimulate molecular pathways, including Nrf2 and PPARγ, which are crucial regulators in the fibrogenesis process.