Portal hypertension (PH) is mainly caused by liver cirrhosis, manifested with gastroesophageal varices (GOV), ascites, hypersplenism and hepatic encephalopathy, etc. PH is a vital sign of decompensated liver cirrhosis and yields poor prognosis. The initial factor of PH is the increase in blood flow resistance in the liver, thereby leading to the formation of visceral hyperdynamic circulation and portosystemic shunts. With the progression of disease, cavernous transformation of portal vein thrombosis (PVT) may occur, which further aggravates hepatic perfusion insufficiency. Hepatic venous pressure gradient (HVPG) is the gold standard for diagnosing and evaluating the severity of PH in liver cirrhosis. HVPG≥10 mmHg (1 mmHg=0.133 kPa) is the clinically significant PH threshold, ≥12 mmHg significantly increases the risk of bleeding, ≥16 mmHg increases the risk of death, and HVPG≥20 mmHg increases the risk of treatment failure and death of esophageal varices bleeding(EVB). The treatment strategy emphasizes staged treatment and multidisciplinary team cooperation. During the compensatory stage, extensive attention is paid to etiological treatment and primary prevention of non-selective β-blocker (NSBB) or endoscopic ligation. The combination of vasoactive drugs and endoscopy is the first choice for acute EVB, and transjugular intrahepatic portosystemic shunt (TIPS) is chosen for patients with treatment failure. NSBB combined with endoscopy or TIPS is recommended for secondary prevention. For patients with recurrent bleeding and acceptable liver function, laparoscopic splenectomy has unique advantages in improving liver function and preventing rebleeding. TIPS bridging or liver transplantation is recommended at the end stage. Individual treatment options should be chosen based on the staging of PH. Efforts should be made to comprehensively consider reducing portal pressure, preventing bleeding and protecting liver function. Anticoagulation and PVT management are the keys to maintaining the continuity of treatment.