The PI3K/AKT signaling pathway plays a critical role in the development and attenuation of liver fibrosis. Liver fibrosis is characterized by the excessive accumulation of extracellular matrix (ECM) components, leading to chronic liver injury. The PI3K/AKT pathway is involved in regulating various cellular processes, including cell survival, proliferation, and metabolism. In the context of liver fibrosis, the pathway has been shown to influence the activation of hepatic stellate cells (HSCs), which are key players in ECM production. Activation of the PI3K/AKT pathway can reduce fibrosis markers and improve liver function by inhibiting HSC activation and ECM synthesis. The pathway also plays a role in regulating oxidative stress and inflammatory responses, which are major contributors to liver fibrosis. Studies have demonstrated that targeting the PI3K/AKT pathway can lead to the attenuation of liver fibrosis through various mechanisms, including the inhibition of profibrogenic gene expression and the modulation of downstream signaling pathways such as TGF-β. Additionally, the PI3K/AKT pathway interacts with other signaling pathways, such as the Nrf2 pathway, to further regulate fibrosis progression. Research has shown that both activation and inhibition of the PI3K/AKT pathway can have therapeutic implications in liver fibrosis, highlighting its potential as a target for the development of effective treatments. The complex interplay between the PI3K/AKT pathway and other signaling pathways underscores the importance of understanding its role in liver fibrosis for the development of targeted therapies.The PI3K/AKT signaling pathway plays a critical role in the development and attenuation of liver fibrosis. Liver fibrosis is characterized by the excessive accumulation of extracellular matrix (ECM) components, leading to chronic liver injury. The PI3K/AKT pathway is involved in regulating various cellular processes, including cell survival, proliferation, and metabolism. In the context of liver fibrosis, the pathway has been shown to influence the activation of hepatic stellate cells (HSCs), which are key players in ECM production. Activation of the PI3K/AKT pathway can reduce fibrosis markers and improve liver function by inhibiting HSC activation and ECM synthesis. The pathway also plays a role in regulating oxidative stress and inflammatory responses, which are major contributors to liver fibrosis. Studies have demonstrated that targeting the PI3K/AKT pathway can lead to the attenuation of liver fibrosis through various mechanisms, including the inhibition of profibrogenic gene expression and the modulation of downstream signaling pathways such as TGF-β. Additionally, the PI3K/AKT pathway interacts with other signaling pathways, such as the Nrf2 pathway, to further regulate fibrosis progression. Research has shown that both activation and inhibition of the PI3K/AKT pathway can have therapeutic implications in liver fibrosis, highlighting its potential as a target for the development of effective treatments. The complex interplay between the PI3K/AKT pathway and other signaling pathways underscores the importance of understanding its role in liver fibrosis for the development of targeted therapies.