Background: A key role for the renin-angiotensin system (RAS) in portal hypertension has been demonstrated in both animal and human . The classical RAS enzyme angiotensin converting enzyme (ACE) is responsible for the conversion of angiotensin I (Ang I) to angiotensin II (Ang II). This, in turn, stimulates hepatic fibrosis, increases intrahepatic vascular tone and portal pressure through stimulation of the Ang II type 1 receptor (AT1R). Although conventional RAS inhibitors, which are commonly used by hypertensive patients, have inhibited liver fibrosis in animal models, sufficiently powered clinical trials have not yet evaluated their effectiveness in human liver disease. These medications may reduce portal pressure, however, can cause off-target side effects including systemic hypotension and kidney failure, according to small studies in cirrhotic individuals.Recent research has linked the alternative RAS—consisting of the enzyme ACE2 and the effector peptide angiotensin-(1-7) (Ang-(1-7)—to the development of liver fibrosis and portal hypertension through the putative receptor Mas (MasR) . It is now widely known that the alternative RAS counter-regulates many of the harmful effects of the ACE-dependent classical RAS; this system is active in both preclinical animal models and human chronic liver disease. Drugs which block the alternate RAS may be useful in treating portal hypertension, according to recent studies. This is because these drugs increase splanchnic vascular resistance in cirrhotic animals, which will improve portal hypertension .With a focus on potential new treatment methods targeting the ACE2-driven alternative RAS, this review highlights the RAS's role in liver fibrosis and portal hypertension.