The article reviews the role of the PI3K/AKT signaling pathway in attenuating liver fibrosis. Liver fibrosis is a pathological condition characterized by excessive accumulation of extracellular matrix (ECM) components, often resulting from chronic liver injuries caused by factors such as alcohol abuse, non-alcoholic fatty liver disease (NAFLD), autoimmune issues, and viral hepatitis. The PI3K/AKT pathway plays a crucial role in regulating cellular processes, including cell survival, proliferation, metabolism, and growth. In the context of liver fibrosis, this pathway is activated in early stages to promote hepatocyte survival and regeneration but becomes blocked as fibrosis progresses, leading to increased ECM production and hepatic stellate cell (HSC) activation. The review highlights several mechanisms through which the PI3K/AKT pathway contributes to the reduction of liver fibrosis. These include inhibiting HSC proliferation and activation, decreasing ECM production, promoting hepatocyte survival and regeneration, controlling oxidative stress, and modulating inflammatory responses. Studies in both in vitro and in vivo models have shown that activating the PI3K/AKT pathway can reduce fibrosis markers and improve liver function. Additionally, the pathway's ability to regulate downstream effectors such as GSK-3β, mTOR, and FOXO3a further enhances its therapeutic potential. The article also discusses the interplay between the PI3K/AKT pathway and the Nrf2 signaling pathway, which together contribute to the regulation of antioxidant responses and the mitigation of liver fibrosis. Furthermore, the review explores clinical and experimental evidence supporting the therapeutic potential of targeting the PI3K/AKT pathway in treating liver fibrosis, including studies using specific agonists and inhibitors. In conclusion, the PI3K/AKT signaling pathway is a promising therapeutic target for liver fibrosis due to its multifaceted mechanisms and potential to improve liver function and reduce fibrosis. Further research is needed to fully understand the underlying mechanisms and identify optimal therapeutic strategies.The article reviews the role of the PI3K/AKT signaling pathway in attenuating liver fibrosis. Liver fibrosis is a pathological condition characterized by excessive accumulation of extracellular matrix (ECM) components, often resulting from chronic liver injuries caused by factors such as alcohol abuse, non-alcoholic fatty liver disease (NAFLD), autoimmune issues, and viral hepatitis. The PI3K/AKT pathway plays a crucial role in regulating cellular processes, including cell survival, proliferation, metabolism, and growth. In the context of liver fibrosis, this pathway is activated in early stages to promote hepatocyte survival and regeneration but becomes blocked as fibrosis progresses, leading to increased ECM production and hepatic stellate cell (HSC) activation. The review highlights several mechanisms through which the PI3K/AKT pathway contributes to the reduction of liver fibrosis. These include inhibiting HSC proliferation and activation, decreasing ECM production, promoting hepatocyte survival and regeneration, controlling oxidative stress, and modulating inflammatory responses. Studies in both in vitro and in vivo models have shown that activating the PI3K/AKT pathway can reduce fibrosis markers and improve liver function. Additionally, the pathway's ability to regulate downstream effectors such as GSK-3β, mTOR, and FOXO3a further enhances its therapeutic potential. The article also discusses the interplay between the PI3K/AKT pathway and the Nrf2 signaling pathway, which together contribute to the regulation of antioxidant responses and the mitigation of liver fibrosis. Furthermore, the review explores clinical and experimental evidence supporting the therapeutic potential of targeting the PI3K/AKT pathway in treating liver fibrosis, including studies using specific agonists and inhibitors. In conclusion, the PI3K/AKT signaling pathway is a promising therapeutic target for liver fibrosis due to its multifaceted mechanisms and potential to improve liver function and reduce fibrosis. Further research is needed to fully understand the underlying mechanisms and identify optimal therapeutic strategies.