Portal hypertension is a serious medical condition arising from the obstruction of normal blood flow within the liver, often associated with conditions like cirrhosis or portal vein thrombosis. In cirrhosis, extensive structural changes occur within the liver, leading to increased resistance to blood flow, a primary driver of portal hypertension. This heightened resistance is a result of factors such as fibrosis and vasoconstriction within the liver. Additionally, alterations in key hepatic cells, like hepatic stellate cells and liver sinusoidal endothelial cells, play pivotal roles in exacerbating this resistance. Furthermore, the dysfunction of these cells can lead to a range of complications, including impaired blood flow control, inflammation, fibrosis, and hindered liver regeneration. Beyond these intrahepatic changes, portal hypertension triggers significant extrahepatic responses. Collateral vessels form to redirect blood from the digestive organs, but this process can lead to serious complications such as variceal bleeding. Additionally, the systemic circulation experiences pronounced arterial vasodilation, increasing blood flow to the portal vein. Understanding these intricate mechanisms is crucial for developing effective interventions to manage and treat portal hypertension.