Role of the renin-angiotensin system in hepatic fibrosis and portal hypertension

Kwang Yong Shim, Young Woo Eom, Moon Young Kim, Seong Hee Kang, Soon Koo Baik

Research output: Contribution to journalReview articlepeer-review

65 Citations (Scopus)


The renin-angiotensin system (RAS) is an important regulator of cirrhosis and portal hypertension. As hepatic fibrosis progresses, levels of the RAS components angiotensin (Ang) II, Ang-(1–7), angiotensin-converting enzyme (ACE), and Ang II type 1 receptor (AT1R) are increased. The primary effector Ang II regulates vasoconstriction, sodium homoeostasis, fibrosis, cell proliferation, and inflammation in various diseases, including liver cirrhosis, through the ACE/Ang II/AT1R axis in the classical RAS. The ACE2/Ang-(1–7)/Mas receptor and ACE2/Ang-(1–9)/ AT2R axes make up the alternative RAS and promote vasodilation, antigrowth, proapoptotic, and anti-inflammatory effects; thus, countering the effects of the classical RAS axis to reduce hepatic fibrogenesis and portal hypertension. Patients with portal hypertension have been treated with RAS antagonists such as ACE inhibitors, Ang receptor blockers, and aldosterone antagonists, with very promising hemodynamic results. In this review, we examine the RAS, its roles in hepatic fibrosis and portal hypertension, and current therapeutic approaches based on the use of RAS antagonists in patients with portal hypertension.

Original languageEnglish
Pages (from-to)453-461
Number of pages9
JournalKorean Journal of Internal Medicine
Issue number3
Publication statusPublished - 2018 May

Bibliographical note

Publisher Copyright:
© 2018 The Korean Association of Internal Medicine.

All Science Journal Classification (ASJC) codes

  • Internal Medicine


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