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

  • Shim, Kwang Yong (Department of Internal Medicine, Yonsei University Wonju College of Medicine) ;
  • Eom, Young Woo (Cell Therapy and Tissue Engineering Center, Yonsei University Wonju College of Medicine) ;
  • Kim, Moon Young (Department of Internal Medicine, Yonsei University Wonju College of Medicine) ;
  • Kang, Seong Hee (Department of Internal Medicine, Yonsei University Wonju College of Medicine) ;
  • Baik, Soon Koo (Department of Internal Medicine, Yonsei University Wonju College of Medicine)
  • Received : 2016.06.27
  • Accepted : 2017.09.05
  • Published : 2018.05.01

Abstract

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.

Keywords

Acknowledgement

Supported by : Yonsei University Wonju College of Medicine, Korea Health Industry Development Institute, National Research Foundation of Korea (NRF)

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