Renin-angiotensin system in the pathogenesis of liver fibrosis.
Hepatic fibrosis is considered a common response to many chronic hepatic injuries. It is a multifunctional process that involves several cell types, cytokines, chemokines and growth factors leading to a disruption of homeostatic mechanisms that maintain the liver ecosystem. In spite of many studies regarding the development of fibrosis, the understanding of the pathogenesis remains obscure. The hepatic tissue remodeling process is highly complex, resulting from the balance between collagen degradation and synthesis. Among the many mediators that take part in this process, the components of the Renin angiotensin system (RAS) have progressively assumed an important role. Angiotensin (Ang) II acts as a profibrotic mediator and Ang-(1-7), the newly recognized RAS component, appears to exert a counter-regulatory role in liver tissue. We briefly review the liver fibrosis process and current aspects of the RAS. This review also aims to discuss some experimental evidence regarding the participation of RAS mediators in the pathogenesis of liver fibrosis, focusing on the putative role of the ACE2-Ang-(1-7)-Mas receptor axis.
Pereira
Regina Maria
RM
Department of Pediatrics, Faculty of Medicine, Federal University of Minas Gerais, Avenue Alfredo Balena, 190, Belo Horizonte, Minas Gerais 30130-100, Brazil.
dos Santos
Robson Augusto Souza
RA
da Costa Dias
Filipi Leles
FL
Teixeira
Mauro Martins
MM
Simões e Silva
Ana Cristina
AC
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D006801:Humans; D008103:Liver Cirrhosis / Q000473:pathology / Q000503:physiopathology*; D010446:Peptide Fragments / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*
D010446:Peptide Fragments; D000804:Angiotensin II