Current intervention strategies for collateral circulation formation and splenomegaly in portal hypertension due to cirrhosis.

Portal hypertension (PH) is a common clinical syndrome characterized by a pathologic increase in portal venous pressure. In cirrhosis, PH occurs owing to extensive fibrosis within the liver parenchyma, causing increased vascular resistance. As PH develops, collateral vessel formation and arterial vasodilation progress, enhancing the blood flow to the portal circulation. Increased levels of circulatory vasodilators are believed to be caused by portosystemic shunting and bacterial translocation, leading to the redistribution of the blood volume with central hypovolemia. Esophagogastric varices and splenomegaly develop as a result of hyperdynamic circulatory syndrome. Cirrhosis-induced blood flow obstruction leads to long-term congestion of the splenic sinus, hyperplasia of fibrous tissue, and proliferation of splenic myeloid cells, culminating in splenomegaly. This condition is a marker of advanced chronic liver disease and PH. Angiogenesis plays a pivotal role in forming portosystemic shunts and splenomegaly. As both jointly reflect the hemodynamic abnormalities in PH, they have become key diagnostic and therapeutic targets. However, significant challenges remain. This review focuses on our current understanding of the pathophysiology of collateral circulation and splenomegaly and novel therapeutic approaches for cirrhosis. Interventions targeting these vascular alterations are expected to exert beneficial effects in managing PH in the future.